Obstetrics and Gynaecology

“I hate” Obstetrics and Gynaecology
TUTORIAL 1: RISK ASSESSMENT IN OBSTETRICS

“A 26-year-old G1P0 woman has twins diagnosed on USS at 8 weeks. Discuss management.”
“A 38-year-old G6P3 woman with previous miscarriages and a stillbirth presents at 36 weeks gestation with
decreased fetal movements. Discuss management.”
• Maternal Risk Assessment

Maternal risk assessment begins at the booking visit and continues with antenatal visits (monthly until 28
weeks, then fortnightly). Between 1/3 and ½ of the women who will subsequently develop problems during
their pregnancy may be identified at their first prenatal visit.
History:
1. General:
a. Age <15 years has higher risk of preeclampsia and underweight or undernourished infants;
age >35 years has higher risk of hypertension, DM, uterine fibroids and labour problems
b. Ethnicity e.g. Asians Æ hepatitis, PI Æ diabetes, African Æ sickle cell, HIV
c. Marital status
2. Gynaecological and obstetric history:
a. Menstrual cycle – regularity, timing, last menstrual period
b. Parity – primigravidae (preeclampsia, preterm labour/delivery), grand multiparous (placenta
praevia, weak contractions, post-partum haemorrhage 2° to uterine atony and rapid labour)
c. Early pregnancy problems – previous ectopic pregnancy (increases risk to 10% c.f. baseline
0.5-1%), miscarriages (3 consecutive increases risk to 40% c.f. 20% baseline)
d. Other complications – preeclampsia, antepartum haemorrhage, multiple pregnancy
e. Delivery – previous preterm delivery (increases risk), previous caesareans and type
3. Medical history (also family history):
a. Hypertension (preeclampsia, abruption, IUGR), diabetes (infection, early labour, high BP),
renal disease (may need early delivery), thyroid disease (fetal hyper- or hypothyroidism),
SLE (miscarriage, IUGR, early delivery), sickle cell disease (infections, high BP), clotting
disorders, fibroids (abnormal presentation, placenta previa, preterm labour, miscarriage)
b. Previous surgery and anaesthetic problems including previous transfusion (Æ group/hold)
c. Medications (e.g. anticonvulsants, warfarin, ACE inhibitors, isotretinoin) and allergies
4. Social history:
a. Smoking Æ IUGR, abruptio placentae, PROM, preterm labour, congenital/developmental
defects. Passive smoking may also harm the fetus and can have effects postnatally.
b. Alcohol is a major cause of birth defects – foetal alcohol syndrome (2.2 per 1000 live births)
is characterised by growth retardation, microcephaly and abnormal behavioural development
c. Other drugs – IV drug users (maternal infectious diseases, IUGR, prematurity), marijuana
(may cause behavioural abnormalities), cocaine (placental abruption)
Examination:
1. General examination:
a. Maternal weight <45kg increases risk of SGA (higher if she gains <6.8kg during pregnancy);
weight >90kg has higher risk of gestational diabetes/hypertension and complications
b. Maternal height <1.52m predicts a small pelvis Æ risk of preterm labour, IUGR
c. General screen – BP, breasts, heart, abdomen, thyroid, deep tendon reflexes
2. Pelvic examination:
a. External – evidence of condylomata acuminata (can Æ neonatal laryngeal papillomas,
anogenital warts), can be treated with cryotherapy or laser but not podophyllin
b. Vagina/cervix – evaluate vaginal discharge (Candida, Trichomonas, bacterial vaginosis) or
cervical discharge (Gonorrhoea, Chlamydia, bacterial vaginosis), smear as appropriate
c. Bimanual to exclude adnexal anomalies; fundal height (should equal gestation – 12/40 at
symphysis, 24/40 at umbilicus, 36/40 at xiphisternum); lie, position and presentation of fetus
Investigations:
1. FBC, blood group and antibody screen (indirect Coombs test)
2. Rubella Ab titre, HBSAg, syphilis serology, high vaginal and endocervical swabs, cervical smear
3. MSU – protein and glucose via dipstick, send off if indicated for UTI
4. USS at 18 weeks for dating and anatomy
© Kevin Luong 2003 1

• Prenatal Risk Assessment
Nuchal translucency is a screening test for chromosomal abnormalities (particularly Down syndrome) and
involves using ultrasound to detect thickening of the skin at the back of the neck. It is done at 11-14 weeks
and results are available immediately – follow-up amniocentesis at 15-17 weeks is recommended if positive.
Maternal serum screening (triple test) stratifies the risk of chromosomal abnormalities (detects 65% of
Down syndrome) or neural tube defects, and involves checking maternal α-FP, oestriol and β-HCG. It is
done at 15-17 weeks, costs ~$75 and results are available in one week.
Amniocentesis is a diagnostic test where a small amount of amniotic fluid is removed under ultrasound
guidance and sent for testing. Tests include chromosome analysis, fetal gender determination and neural
tube defect detection (amniotic fluid α-FP). It is done at 15-17 weeks and results are available within 3
weeks. It is relatively safe, but does carry a small (~1%) risk of miscarriage above baseline.
Chorionic villus biopsy involves obtaining a small sample of the placenta under ultrasound guidance for
testing. It is done at 11-14 weeks and results are available in 2-3 weeks. Occasionally a result will not be
available due to technical reasons Æ refer for amniocentesis. Risks are similar to amniocentesis.
TUTORIAL 2: EARLY PREGNANCY PROBLEMS

• Nausea and Vomiting in Pregnancy
“A 22-year old Samoan women presents with nausea and vomiting at 8 weeks gestation in her second
pregnancy. Discuss management.”
Common symptoms in the first 10 weeks of pregnancy include nausea, vomiting, bladder irritability and
breast enlargement. Other symptoms occurring throughout pregnancy include:
1. Cardiovascular – haemorrhoids, varicose veins, peripheral vasodilatation (headache, sweating, faint)
2. Gastrointestinal – constipation, nausea and vomiting, reflux,
3. Genitourinary – urinary incontinence/frequency, thrush
4. Neurological – backache (3rd trimester), altered taste sensation
5. Others: oedema, carpal tunnel syndrome (2° to fluid retention), cramps, striae gravidarum, chloasma
Hyperemesis gravidarum is sustained nausea and vomiting for at least three weeks, occurring before 12
weeks gestation. It only affects 1 in 1000 pregnancies but can have significant consequences.
1. Risk factors – young, non-smoker, primiparity, family history, working outside of home, multiple or
molar pregnancy (excessive β-HCG levels may have an aetiological role)
2. Clinical features – inability to keep food/fluids down, weight decreased by 2-5kg, dehydration,
hypovolaemia, electrolyte disturbance with hyponatraemic shock, polyneuritis (decreased B
vitamins), behavioural disorders, liver and renal failure
3. Investigations:
a. PCV and U&Es to help guide management of electrolyte disturbance
b. TFTs looking for associated thyroid or adrenal dysfunction
c. MSU to exclude UTI
d. USS to exclude twin pregnancy or hydatidiform mole
4. Management:
a. Admit to hospital Æ IV rehydration + K+, thiamine and folate supplementation
b. Drug treatment should be avoided during organogenesis (first 8 weeks) but in general most
women require regular metoclopramide or antihistamine antiemetics (? role of steroids)
c. Severe cases may require NG feeds or even TPN
• Bleeding in Early Pregnancy

“A women who suspects she is pregnant is admitted to hospital with some vaginal bleeding, pallor and
abdominal pain. What is wrong, and what would you do?”
Clinical approach to early pregnancy bleeding:

1. History:
a. Presenting complaint – how much blood, pattern, associated pain or cramping
b. Menstrual history – LMP (timing and character), previous menstrual period, usual interval
c. Medications – OCP, other drugs
d. Past medical history – diabetes, thyroid disorders, SLE etc
e. Past obstetric history – past abortions/miscarriages (spontaneous or induced), complications
f. Past gynaecological history – smears, STDs
2. Physical examination:
2 © Kevin Luong 2003

a. Vital signs – signs of hypovolaemia or sepsis
b. Abdomen – tenderness, bloating, peritonism (from bleeding)
c. PV exam – identify source of bleeding, swab as appropriate, check adnexal tenderness
3. Investigations
a. FBC, Rh typing, antibody screen
b. β-HCG is first detectable 9-11 days after ovulation, reaching ~100mIU/mL at the expected
time of menses and doubling every 72 hours in a viable pregnancy. Levels increase until
week 10, then decline until the 3rd trimester where they gradually climb again.
i. Serial measurements are fairly handy – a peak, plateau or fall suggests a problem
ii. High values may correlate with multiple or molar pregnancy or rarely an ovarian
tumour; slow-rising values occur in abnormal intrauterine and ectopic pregnancies
c. USS allows a definitive diagnosis in many cases, guiding treatment
i. Transvaginal USS should detect a gestational sac at a β-HCG of 1500mIU/mL, while
a transabdominal scan may not detect a sac until β-HCG reaches 6000mIU/mL
ii. If β-HCG is above these levels but no sac is visible, an ectopic location is assumed
iii. Also useful for confirming a hydatidiform pregnancy (diffuse vesicular mass)
Implantation bleeding occurs when the trophoblast implants into the endometrium and the maternal blood
supply. Clinically this bleed is bright red and of short duration – it occurs 8-12 days post-fertilisation (typically
just before the menstrual period would normally be due).
Ectopic pregnancy is defined as implantation outside the uterine cavity – it is the major cause of maternal
mortality before 20 weeks. 95% are in the fallopian tubes (1 in 150 pregnancies; due to delayed passage of
the zygote due to a congenital or acquired damage); other sites include the ovary, pelvic peritoneum and
uterine cornu. Only 50-60% of women will conceive again, and 10% of subsequent pregnancies are ectopic..
1. Risk factors – West Indians, some Africans, maternal age, low parity, history of previous surgery,
hormonal stimulation of ovulation, salpingitis, IUCD, tubal endometriosis, PID, progestogen-only pill
2. Clinical features:
a. History – irregular vaginal bleeding or amenorrhoea (though 40% do not miss a period),
sudden lower abdominal pain, shoulder-tip pain, dizziness and syncope, pain on defaecation
b. Examination – pelvic tenderness, adnexal mass (50%), peritonism and shock (if ruptured)
c. Investigations:
i. β-HCG >6000IU/L diagnostic with transabdominal USS (empty uterus); β-HCG
>1500IU/L diagnostic if transvaginal used (note that 70% present lower than this)
ii. Laparoscopy indicated if patient deteriorating, adnexal mass ± peritoneal fluid, and
USS is non-diagnostic and β-HCG >1000IU/L
3. Management:
a. Supportive – IV fluids, group and hold, cross-match 6 units
b. Medical – methotrexate (folate antagonist) if mass unruptured and <4cm diameter
c. Surgical – laparoscopy or laparotomy
Miscarriage is defined as the loss of a pregnancy before 24 weeks gestation. It is the most common
complication of pregnancy – 25% of conceptions are miscarried before pregnancy is recognised, and 15% of
recognised pregnancies end in miscarriage.
1. Aetiology:
a. Detectable chromosomal anomalies (50%) – monosomy X, trisomy, triploidy and tetraploidy
b. Structural anomalies – e.g. neural tube defects
c. Maternal factors (2nd trimester onwards) – cervical incompetence, uterine abnormalities
2. Risk factors
a. Intrinsic factors – maternal age, prior miscarriage/infertility, uterine/cervical abnormalities
b. Maternal disease – infection (Toxoplasma, CMV, Listeria), anti-phospholipid syndrome
c. Social – tobacco or EtOH intake, environmental or occupational stress
d. Iatrogenic – IUD at conception, CVS or amniocentesis
3. Classification:
a. Threatened miscarriage – any bleeding in the first 20 weeks without passage of tissue or
cervical dilatation (note that inconsequential bleeding occurs in 20% of normal pregnancies)
i. Poor prognostic signs – bleeding worse than menstruation, pain
ii. Fetal heart is detectable on USS by 6 weeks – 95% of pregnancies continue if seen
iii. Preterm labour, antepartum haemorrhage and IUGR are more common in this group
b. Inevitable miscarriage – characterised by bleeding, pain and an open cervix
i. Gestational sac separates Æ ↑bleeding, contractions similar to labour
ii. A blighted ovum (empty sac) at >7 weeks means that miscarriage is inevitable
iii. USS to confirm diagnosis, repeat in 3 days to determine need for evacuation

c. Missed miscarriage – fetus dies in utero but the products of conception are retained
i. Pregnancy symptoms decline, brown discharge ± bleeding, uterus small for dates
ii. USS confirms fetal death Æ evacuation by suction or misoprostol 600μg
d. Recurrent miscarriage – consecutive loss of >3 early pregnancies, affecting 1% of women
i. Aetiology – idiopathic (50%), parental chromosomal abnormalities, antiphospholipid
syndrome, PCOS, defective luteal phase, uterine anomalies, cervical incompetence
ii. 80% eventually delivery a baby when managed in specialist clinics
iii. Prognosis is improved with young maternal age and only 3 miscarriages
4. Follow-up:
a. Miscarriage often represents the loss of a carefully planned and eagerly awaited child.
Feelings of guilt and blame must be talked through, and discussion of causes is essential.
b. If a recognisable fetus is delivered, parent often want to view/hold/bury/cremate the baby
c. Contraception must be discussed on discharge – the next pregnancy should not be
attempted until 2 normal periods have occurred
d. Others – advise women to stop smoking and drinking EtOH, folic acid (8μg od) supplements
Hydatidiform mole is the result of degeneration of grossly swollen chorionic villi with abnormal trophoblastic
tissue – the embryo usually dies and is reabsorbed. Incidence is 1.5 in 1000 pregnancies, with higher rates
in Asians and Mexicans, women <20 and >40 years of age, multiparous women and smokers.
1. Classification:
a. Complete mole – 46XX, all chromosomes paternal (occasionally 2 sperm Æ 46XY)
b. Partial mole – normally triploid chromosomes (normal ovum with diploid sperm or 2 haploid
sperm); some vesicles within an otherwise normal placenta
a. Strong pregnancy symptoms ± bleeding (at ~12 weeks; profuse when mole aborts)
b. Abdominal pain 2° to theca-lutein cysts which may take up to 4 months to resolve
c. Uterus is large, soft and doughy – no fetal heart on USS with ‘snowstorm’ appearance
d. β-HCG higher than normal pregnancy, may lead to thyrotoxicosis (similar α-chain as TSH)
3. Management:
a. Evacuation by suction, then curettage (can cause heavy bleeding – syntocin may help)
b. Follow-up – CXR to detect pulmonary lesions of choriocarcinoma (3% risk); β-HCG levels
fortnightly until negative, then monthly for a year. Avoid pregnancy for period of follow-up.
Choriocarcinoma is a malignancy of trophoblastic tissue that occurs in 1:30,000 pregnancies – 50% are
from complete hydatidiform moles, 25% from spontaneous abortions or partial moles, and 25% from term
deliveries (may be many years after pregnancy). There may be general malaise (elevated β-HCG), uterine
bleeding, or signs and symptoms of metastases (lung, vagina, pelvis, brain, liver). They are very sensitive to
chemotherapy (methotrexate alone or in combination) and prognosis is excellent.
Other causes of early pregnancy bleeding include cervical lesions (ectropion, polyps, cancer) and vaginitis.
TUTORIAL 3: HYPERTENSION IN PREGNANCY

“A primigravid woman presents with frequent headaches at 32 weeks and has a BP of 130/100mmHg and 1+
proteinuria. At booking (12 weeks) BP was 110/60 with no proteinuria. Discuss management.”
Hypertension in pregnancy is a common complication of pregnancy, occurring spontaneously in 8-10% with

preeclampsia in 3-5% of pregnancies. It is a major cause of maternal and perinatal morbidity/mortality, abut
is unpredictable in its onset, progress and complications.
Key definitions:
• Hypertension – on two occasions at least 6 hours apart, a systolic BP 140mmHg or diastolic BP
90mmHg (probably more useful) or an increase of 30mmHg systolic or 15mmHg diastolic
• Gestational hypertension – hypertension arising in and induced by pregnancy (c.f. chronic HT)
• Pre-eclampsia – development of hypertension in pregnancy with one or more of the following:
a. Proteinuria: dipstick +1, 300mg/L in 24hr urine or urine protein/creatinine ratio >30mg/mmol
b. Renal insufficiency: oliguria or serum/plasma creatinine >0.09mmol/L
c. Liver disease: epigastric/RUQ pain and/or elevated serum transaminases (AST/ALT)
d. Neurological: visual disturbances, severe headaches, hyperreflexia with clonus, convulsions
e. Haematological: thrombocytopaenia, disseminated intravascular coagulation
In pregnancy, cardiac output normally increases by 30-50% and peripheral resistance normally decreases by
25%. In pre-eclampsia cardiac output still increases, but peripheral resistance also increases leading to

increased blood pressure. It is thought that there is damage to the maternal endothelium (mediated by
prostaglandins released from an ischaemic placenta), leading to increased maternal vascular reactivity,
vasoconstriction, increased capillary permeability and ultimately disseminated intravascular coagulation.
• Clinical Features
Risk factors include:
1. Extremes of age (<20 or >35 years)
2. Obstetric – nulliparity, primigravid, multiple pregnancy (3x risk), donor sperm/oocyte pregnancies
3. Personal or family history of gestational hypertension or pre-eclampsia
4. Underlying medical conditions – essential hypertension, renal disease, DM, SLE/APL, thrombophilia
Assessment – note that pre-eclampsia is often asymptomatic and picked up on routine testing.
1. Symptoms:
a. Maternal – headache, visual disturbance, epigastric/uterine pain, vaginal bleeding
(abruption), breathlessness (pulmonary oedema), convulsions
b. Fetal – decreased movements (e.g. decreased frequency or strength of kicking)
2. Signs:
a. Maternal – oedema or weight gain (>0.5kg/week), elevated BP, hyperreflexia and clonus
b. Fetal – decreased baseline variability and decelerations on CTG, decreased liquor volume,
decreased heart rate, decreased growth on USS
3. Investigations:
a. Maternal – FBC (↑haematocrit, ↓platelets), U&Es (↓CrCl, ↑serum Cr), LFTS (↑AST, ↑ALT,
↓albumin), 24-hour urine (proteinuria >0.3g/24h); urine microscopy/culture (to exclude UTI)
b. Fetal – USS, CTG, biophysical profile, umbilical artery Doppler (assess blood flow velocity)
Complications of preeclampsia include HELLP syndrome (haemolysis, elevated liver enzymes, low platelets
– actually just preeclampsia with multisystem disease) and eclampsia, where there are seizures that put both
the mother and fetus at risk. Reduced perfusion to peripheral tissues leads to ischaemia in the maternal
brain, liver and kidneys and also the placenta and fetal organs (e.g. kidney Æ oligohydramnios). Other
complications include IUGR, placental abruption, premature birth and perinatal mortality.
• Management
Management of preeclampsia should aim to prevent convulsions, prevent complications, and deliver a
healthy child with minimal trauma to the mother. Note that there are no proven therapies to prevent pre-
eclampsia, although low-dose aspirin might help (really needs specialist referral though).
1. Antihypertensive therapy basically reduces maternal risk (aim for diastolic of 90-100mmHg). It is
indicated if BP >170/110mmHg, and should be considered if BP >160/110mmHg.
a. 1st line – methyldopa, oxprenalol, labetalol (α and β blocker)
b. 2nd line – nifedipine (Ca+2 antagonist), hydralazine (used in eclampsia – fast onset)
c. 3rd line – prazosin, clonidine
d. Avoid ACE inhibitors (IUGR, neonatal renal failure and fetal death), angiotensin II receptor
antagonists and diuretics (decrease the already low plasma volume)
2. Anticonvulsant therapy:
a. MgSO4 iv/im is used prophylactically in severe pre-eclampsia or when convulsions have
already occurred (rare – terminate ongoing convulsions with diazepam 5-20mg iv)
b. Levels need to be carefully monitored – early signs of toxicity include nausea, warmth,
flushing, double vision, slurred speech, weakness, loss of patellar tendon reflex; followed by
muscular paralysis, respiratory arrest and finally cardiac arrest
c. MgSO4 may be revered with 10% calcium gluconate and nasal oxygen
3. Timely delivery:
a. Pre-eclampsia is effectively cured by delivery of the placenta, though if multisystem disease
is present prior to delivery there may be further deterioration over 24-72 hours post-partum
b. If pre-eclampsia occurs pre-term (<37 weeks), consider steroids and deliver if indicated:
i. Maternal: inability to control BP (despite 3+ drugs), deteriorating liver/renal function,
progressive thrombocytopaenia, neurological complications, pulmonary oedema
ii. Fetal – placental abruption, fetal distress on CTG or biophysical profile
c. Antihypertensive therapy should continue throughout labour – epidural may be helpful to
reduce elevations in blood pressure 2° to pain; do not use ergometrin in 3rd stage (raises BP)
4. Follow-up:
a. Careful monitoring in the first 48 hours post-partum is required and usually involves blood
tests and clinical assessment every 4-8 hours in unstable women
b. Investigate for residual hypertension and any underlying disorders as appropriate

TUTORIAL 4: DIABETES IN PREGNANCY
“An insulin dependent diabetic aged 18 says she would like to become pregnant next year. She asks
whether her diabetes is a problem and what she can do to prepare for pregnancy.”
“A G4P2 woman has an abnormal Polycose screening test at 28 weeks gestation. What are the implications
of this and what is your management plan?”
Key definitions:
• Gestational diabetes mellitus (c.f. pre-existing DM) – glucose/carbohydrate intolerance with onset or
first recognition during pregnancy, occurring in 5.5-8.8% of pregnant women.
• Glucose Metabolism in Pregnancy

Pregnancy is characterised by a hyperinsulinaemic state and a decrease in insulin sensitivity:
1. In early pregnancy oestrogens and progesterone induce β-cell hyperplasia, increasing insulin levels
2. As pregnancy progresses there is increasing tissue insulin resistance, while increased human
placental lactogen promotes maternal lipolysis (reserving glucose and amino acids for the fetus)
3. There is usually sufficiently elevated insulin to offset insulin resistance – however, if the pregnant
woman has borderline pancreatic reserve or is obese (i.e. insulin resistant) levels may be insufficient
a. This manifests as maternal then fetal hyperglycaemia – often recurrent post-prandial attacks
b. Episodic fetal hyperinsulinaemia also promotes nutrient storage Æ macrosomia, hypoxia
c. Episodes of fetal hypoxia are accompanied by surges in adrenal catecholamine levels which
cause hypertension, cardiac remodelling, stimulation of EPO and red cell hyperplasia
Risk factors include:
1. >30 years of age, >90kg weight, PCOS, family history of diabetes (first degree relative)
2. Previous GDM, LAG baby, unexplained stillbirth or spontaneous miscarriage
3. Glycosuria on >2 occasions, fasting or random blood glucose >7mM
4. Ethnicity: high risk (Maori, Pacific Islander), moderate risk (Indian, Asian, Middle Eastern)
Complications of diabetes mellitus in pregnancy include:

1. Maternal:
a. Diabetic crises: hypoglycaemia (first half of pregnancy), hyperglycaemia, ketoacidosis
b. Obstetric: preterm labour (50%), caesarean section, shoulder dystocia, pre-eclampsia (12%)
c. End-organ damage:
i. Cardiac – high myocardial demand and inadequate oxygenation Æ MI, arrhythmias
ii. Renal – nephropathy Æ hypertension, prematurity, IUGR, perinatal mortality
iii. Ophthalmic – retinopathy accelerated (regresses 6/12 post-partum), beware labour
d. Long-term – gestational diabetes recurs in 20-50% of subsequent pregnancies; 50%
develop full-blown type 2 diabetes within 15 years
2. Fetal/neonatal:
a. Mortality – 4-5x risk of intrauterine death (usually after 36/40), 2x risk of perinatal mortality
b. Growth – macrosomia (15-45%), small for gestational age (20%, mainly 2° to nephropathy)
c. Congenital malformations – 4-8x increased risk (relating to periconceptual glycaemic control)
d. Neonatal – respiratory distress syndrome, transient tachypnoea of the newborn,
hypoglycaemia, polycythaemia, hyperbilirubinaemia, hypocalcaemia, hypomagnesaemia
• Screening Tests for Gestational Diabetes

A fasting glucose of >5.5mmol/L is diagnostic of gestational diabetes – otherwise all pregnant women are
screened at 24-28 weeks with a one-hour post-Polycose test (50g glucose) which has a sensitivity of ~80%:
1. Blood glucose of >7.8 – a two-hour glucose tolerance test (75g in 300mL water) confirms diagnosis
of gestational diabetes mellitus if glucose is >9mmol/L
2. Blood glucose of 7.0-7.7 – provide dietary advice, repeat test in 4 weeks
Testing may be done earlier in patients who have glycosuria (on >2 occasions), a first degree relative with
diabetes mellitus, a LGA baby, previous unexplained perinatal death, maternal obesity or polyhydramnios. If
screening is normal in early pregnancy, tests are generally repeated at 26-30 weeks.
There is some debate as to whether screening is warranted, and it certainly has some limitations – it is
expensive, time-consuming, unpleasant (especially in pregnancy), non-physiological, not related to body
weight, variable in terms of predictive value (with ethnicity) and up to 24% of results are not reproducible.

• Management
Pre-pregnancy management (women with overt diabetes mellitus or previous history of GDM):
1. Counselling – explain general risks of diabetes in pregnancy, encourage development of supports
2. Assessment – perform risk assessment, refer appropriately and check rubella status
3. Glucose control – replace hypoglycaemics with insulin; ideally HbA1c <7% for 3/12 before pregnancy
4. 5mg folic acid per day for 3/12 prior to conception and during the first trimester
Antenatal management should be coordinated in a specialist multidisciplinary clinic, involving an

obstetrician, clinical nurse specialist, dietician, paediatrician and midwife.
1. Education should include implications of diabetes on the mother and baby, dietary and exercise
recommendations, and importance of blood glucose monitoring
2. Conservative management – diet and exercise (30 minutes after meals):
a. At least 1800 calories (30cal/kg of ideal body weight + 300 calories for weight gain) as 50-
55% carbohydrates, 10-15% protein, 30-35% fat (<1/3 saturated fats)
b. Adjust diet according to weight gain, insulin requirements and exercise pattern e.g. may
need more calories in obese patients to prevent starvation ketoacidosis
3. Insulin is added to diet if blood glucose goals (fasting <5.5mM, 1h <8mM, 2h <7mM) are not met on
more than 2 occasions within a 1-2 week interval (especially if suspicious of macrosomia)
a. Use short-acting insulin 30-45 minutes prior to meals and intermediate-acting before bed
b. Oral hypoglycaemics are not used as they can cross the placenta Æ fetal hypoglycaemia
4. Follow-up:
a. Monthly MSU and blood pressure
b. Each trimester – examine fundi, measure HbA1c, check renal function if indicated
c. GDM needs biophysical profile testing weekly from 10 to 37 weeks, then twice-weekly
following; pre-existing diabetes needs fortnightly fetal testing from 34 weeks
Intrapartum management:
1. Induce at 38/40 if there is poor glucose control, pre-eclampsia or other maternal/fetal complications
2. Consider elective caesarean section in women with a history of infertility/miscarriage, poor diabetic
control, vascular complications or if estimated fetal weight is >4.2kg
3. Aim for vaginal delivery within 12 hours – maintain maternal normoglycaemia with 10% dextrose
infusion at 100mL/hr with 1-2 units of insulin per hour; check plasma glucose hourly (4.5-5.5mmol/L)
Post-partum management:
1. Maternal:
a. Insulin needs fall as the placenta is the source of many insulin antagonists. Insulin is started
after 48-72 hrs (sliding scale) as oral hypoglycaemics are contraindicated in breastfeeding
b. Repeat OGTT 6-8 weeks post-partum, then at least 2-yearly (more frequent if higher risk)
2. Neonatal:
a. Assess carefully for perinatal complications; breast feed as early as possible
b. Take blood glucose at 1hr and before feeds until three feeds >2.6mmol/L – if hypoglycaemic
use 10% dextrose at 2mL/kg over 5 minutes then 6-8mL/kg/minute until normoglycaemic
TUTORIAL 5: ANTEPARTUM HAEMORRHAGE

“A 28-year-old woman is pregnant with her third child. At 31 weeks she has an antepartum haemorrhage of
150mLs. What is the differential diagnosis and treatment?”
Key definitions:
• Antepartum haemorrhage – bleeding from the genital tract after 20 weeks of gestation until onset of
labour (including the first and second stages of labour). Causes include:
o Placental – edge bleeding, placenta praevia, placenta abruption, vasa praevia
o Local – cervicitis, cervical erosions/carcinoma, vaginal trauma/infection
o Others – bloody show, uterine rupture
• Placenta Praevia
Placenta praevia occurs when the blastocyst implants entirely or partly on the lower uterine segment. It is a
cause of painless, recurrent vaginal bleeding occurring in less than 1% of term deliveries. Bleeding occurs
when uterine contractions place shear forces on the placental attachment – separation may also be due to
digital examination of the cervix or rectum, though using a speculum is acceptable.
1. Classification – grade I and II are considered minor and can be delivered normally, while grade III
and IV are considered major and require caesarean sections. Neither may bleed until labour occurs.
a. Grade I – placenta encroaches on lower segment but doesn’t reach the internal os

b. Grade II – placenta reaches internal os but does not cover it
c. Grade III – placenta does cover the internal os, but would not do so at full dilation
d. Grade IV – placenta completely covers internal os and is judged that it would at full dilation
2. Aetiology:
a. Specific cause is unknown – some believe it is purely idiopathic while others believe there is
some contribution from previous uterine damage
b. Risk factors include multiple pregnancy, older multiparous women and those who have
previously had caesarean sections.
c. There is also slightly increased risk with previous dilation and curettage and spontaneous
abortion, and those who have had retained products of conception removed.
a. Repeated ‘spotting’ (bright red blood, painless) as the lower segment forms (usually <28/40)
b. Fetus has an abnormal lie (transverse, oblique or unstable) due to the placental position
c. On examination there is a soft, non-tender uterus and high presenting part in late pregnancy
d. USS is used for diagnosis, though is really only accurate transvaginally in the third trimester
4. Management is non-specific, though tocolytics can be used to prevent contractions. Note that any
bleeds require admission to hospital for at least 48 hours as there is risk of re-bleeding.
a. Minor – aim for vaginal delivery as an outpatient; establish red cell antibody status and give
anti-D prophylactically; review immediately if bleeding occurs
b. Major – caesarean section is mandatory; watch for post-partum haemorrhage (placenta on
poorly contracting uterine muscle); coitus is proscribed
• Placental Abruption
Placental abruption is a progressive and severe condition where there is haemorrhage between the
placenta and the uterine wall. Bleeding may be concealed or may present with visible vaginal bleeding as
the accumulating clot causes separation of the placenta until the edge is reached. Typically the blood tracks
through the myometrium causing intense contractions, severe pain and shock – reduced O2 perfusion and
uterine spasm compromises the placenta leading to fetal complications.
1. Aetiology:
a. Risk factors: maternal age, previous abruption, pre-eclampsia (unclear if hypertension is a
cause or effect), high parity, uterine fibroids, smoking, alcohol use, cocaine use and trauma
b. Maternal disease such as diabetes and collagen diseases that may cause vascular injury
are associated with increased incidence of placental separation
c. Precipitating factors include trauma (particularly RTCs), sudden uterine decompression from
rupture of membranes or delivery of a first twin, and traction on a short umbilical cord
a. Abdominal pain with tender/spasmodic uterus
b. Vaginal bleeding (old blood) accompanied by severe shock out of proportion to visible loss
c. Fetal parts hard to palpate – CTG shows rapid contractions, fetal distress
d. 10% have ↓fibrinogen, ↓platelets, ↓clotting factors; ↑fibrin degradation products and ↑INR
3. Management depends somewhat on whether the fetus is alive – if the fetus is dead, conservative
measures may be sufficient until the mother goes into labour spontaneously.
a. Treat the shock – narcotic pain relief, oxygen, cross-match 6 units of blood, restore blood
volume, monitor urine output (renal failure secondary to DIC)
b. Deliver the fetus – by caesarean section if fetus is alive and near full gestation; or by artificial
rupture of membranes if the cervix is ripe or the fetus is dead
c. Treat DIC – urgent haematology referral, check platelets, give FFP/fresh blood if available
Placental edge bleeding is a form of placental abruption where the detachment is marginal rather than
central (often occurring with a circumvallate placenta). There is only minor recurrent bleeding and the lesion
does not extend, so there is minimal risk to fetus or mother. Treatment is by bed rest and monitoring of
haemoglobin to ensure adequate reserve – note that placenta praevia must be excluded.
• Other Causes of Antepartum Bleeding

Vasa praevia is a rare but serious complication that results in fetal exsanguination. It occurs when the
umbilical vessels pass in front of the internal os before the presenting part, leading to compression or rupture
and fetal distress or mortality.
1. Risk factors include a succenturiate placenta (accessory lobe), velamentous insertion of the
umbilical cord (c.f. central/eccentric/battledore) and separate umbilical vessels (no Wharton’s jelly).
2. Usually presents with vaginal bleeding at the time the membranes rupture; Kleihauer test can
indicate whether the blood is of fetal origin
3. Treatment is by immediate caesarean, though if the fetus is dead it can be born vaginally

Uterine rupture may be complete (full thickness including the serosal peritoneum) or incomplete
(dehiscence of uterine incision – visceral peritoneum remains intact).
1. Risk factors include prior hysterostomy, trauma, uterine overdistension, uterine anomalies, placenta
accreta/increta/percreta and choriocarcinoma. Improper oxytocin administration may be related.
2. Presents with suprapubic pain, cessation of uterine contractions ± a tearing sensation, vaginal
bleeding or haematuria, recession of the presenting part and disappearance of fetal heart sounds
3. Treatment is usually by hysterectomy – maternal mortality is 4.2%; fetal mortality is ~46%
TUTORIAL 6: THE SMALL FOR DATES PREGNANCY AND ASSESSMENT OF FETAL WELL-BEING
“You see a 32-year-old woman in Antenatal clinic. She has just had a scan and the midwife who saw her
last week thought the baby felt a bit small. The scan shows the baby is not growing as well as expected.”
Key definitions – note that these terms are not interchangeable (imagine a Venn diagram)
• Small for gestational age (SGA) – babies with a birth weight below the 10th centile (or 2 standard
deviations) for their gestational age for whatever reason (but including normal genetic factors)
o 40% are constitutionally and statistically small but otherwise healthy neonates
o 20% are abnormally and intrinsically small e.g. trisomy 18, CMV infection, fetal alcohol
o 40% are truly growth restricted and may benefit from appropriate prenatal intervention
• Intrauterine growth restriction (IUGR) – a condition in which a fetus is unable to grow to its
genetically determined potential size to a degree that may affect the health of the fetus
o 20% are symmetric with a relatively proportionate decrease in many organ weights, thought
to be due to a period of poor intrauterine growth secondary to an endogenous defect
o 80% are asymmetric where there is relative sparing of brain weight, especially compared to
liver or thymus, thought to be due to utero-placental insufficiency (that may be treatable)
• Aetiology and Complications

Aetiology – note that a cause may not be identified in as many as 40% of cases:
1. Fetoplacental causes:
a. Genetic disorders – trisomy 21, 18, 13; Turner’s syndrome; neural tube defects, dysmorphic
syndromes, abdominal wall defects, renal anomalies, other autosomal recessive syndromes
b. Congenital infections – CMV, rubella, herpesviruses, VZV, listeriosis, toxoplasmosis, malaria
c. Placental disorders – placenta previa, infarction, chorionic villitis, chronic partial separation,
malformations (circumvallate placenta, battledore placenta, placental haemangioma)
d. Multiple gestation – placental insufficiency, twin-twin transfusion syndrome, other anomalies
2. Maternal causes:
a. Maternal disease – hypertension, anaemia, renal disease, malnutrition, autoimmune disease
b. Drugs – EtOH, tobacco, cocaine, heroin, warfarin, folic acid antagonists, anticonvulsants
c. Maternal features – smaller women have smaller infants (reduced uterine growth potential)
d. Gender – female fetuses are 5% (150g) smaller and 2% (1cm) shorter than male fetuses
Complications:
1. Maternal – preeclampsia, premature labour, induction of labour, caesarean delivery
2. Fetal – stillbirth, hypoxia/acidosis, ischaemic encephalopathy, fetal compromise in labour
3. Neonatal – hypoglycaemia (↓ fat stores), hypocalcaemia, hypoxia/acidosis, temperature instability,
polycythaemia, thrombocytopaenia, meconium aspiration, pulmonary haemorrhage, sepsis
• Assessment and Investigations

Assessment of whether a fetus is small for gestational age depends on the accurate determination of
gestational age (best by LMP if known) and the recognition of fetal smallness (maternal weight gain helpful):
1. If dates are uncertain, obtain two points on the growth curve. If growth is parallel to a standard curve
over two weeks and all other evaluations are normal, the fetus is probably just constitutionally small.
2. Women with conditions associated with IUGR should have serial sonography during pregnancy, at
least at 18-20 weeks and at 28-32 weeks to detect abnormal growth, asymmetry and anomalies.
3. Women without these conditions should be screened with symphysis-fundal height measurements –
a discrepancy of >3cm between observed and expected measurements is an indication for USS
Investigations:
1. Fetal surveillance – antenatal visits with physical examination and NST or CST weekly, ultrasound
every 4-6 weeks, amniotic fluid volume as indicated (at least weekly in at-risk pregnancies)
a. Maternal assessment of fetal movement: >4 in 1 hour, or 2-3 hours to reach 10 movements
b. Nonstress test (NST, CTG): reactive test is very predictive of low fetal mortality in 72-96hrs

c.Biophysical profile: CTG, amniotic fluid volume, fetal tone, movement, and breathing scored
0 or 2; >8 is reassuring, 6 is concerning (repeat in 6-24hrs), 4 is trouble (consider delivery)
d. Ultrasonography: crown-rump length, biparietal diameter, head circumference, abdominal
circumference and femur length converted to fetal weight estimates plotted on growth curve
i. Oligohydramnios also occurs in IUGR (80-90% of cases) and may be the earliest
sign detected on ultrasound (thought to be 2° to decreased renal perfusion)
ii. Doppler is used to observe blood flow in the uterine, umbilical (retrograde diastolic
flow) and fetal cerebral circulation. Not useful for screening but helpful to reduce
intervention and improves overall fetal outcome in IUGR pregnancies
2. Maternal screening
a. If at risk – FBC, U&Es, LFTs, 24-hour urine (creatinine clearance, total protein)
b. Maternal serum α-fetoprotein – elevation predictive of increased risk for mother and fetus
c. Exclude infection if indicated – immune status (IgG against CMV, rubella, Toxoplasma)
d. Others – BP, chorionic villus sampling (11-14/40), amniocentesis (15-17/40), cordocentesis
Note that no single measurement is completely accurate for making or excluding the diagnosis of growth
restriction – the fetal diagnosis is always presumptive as 1) accuracy of predicting birth weight by ultrasound
is ± 10% at best, 2) not all fetuses who are SGA have IUGR, 3) individual and unpredictable changes in
growth potential do occur, and 4) growth distribution is a continuum and borderline individuals exist.
• Management and Prognosis

Pre-labour management of IUGR is somewhat limited since many of the causes are non-preventable. Also,
once IUGR is established, no therapy has been proven to allow catch-up growth in utero.
1. Treatment of impaired growth – one meta-analysis reported that only the following are useful:
a. Behavioural strategies for smoking cessation result in fewer low birth weight babies at term
b. Balanced nutritional supplements, Mg+2 and folate may decreases the rate of SGA newborns
c. If malaria is the aetiologic agent, treatment can increase growth (in-hospital bedrest doesn’t)
d. Chronic tocolytic therapy (decreased uterine tone Æ improved perfusion) doesn’t help
2. Reduction of perinatal morbidity and mortality:
a. Bed rest maximises uterine blood flow, so may be useful for asymmetric IUGR fetuses
b. Maternal hyperoxygenation (experimental) reduces fetal mortality from 55-85% to 20-29%
c. Others (poorly studied) – maternal haemodilution, intermittent abdominal negative pressure
3. Prophylaxis using aspirin ± dipyridamole (altering the thromboxane-to-prostacyclin ratio to prevent
idiopathic uteroplacental insufficiency) has been suggested but the role of this is still unclear
Management during labour and the puerperium should aim to deliver the most mature fetus in the best
condition possible with minimal risk to the mother. This relies heavily on antenatal testing to identify the
IUGR fetus before it becomes acidotic – having a high index of suspicion is important.
1. Each IUGR pregnancy needs to be assessed individually to determine the optimal time of delivery
(the point where the baby will do as well outside as it would have inside the uterus)
a. Indications – fetal maturity, fetal compromise or gestational age of 38 weeks
b. IUGR may or may not accelerate lung maturity, so give steroids to deliveries <34/40 in case
2. Delivery should take place somewhere where obstetric care, anaesthesia and neonatal care are
readily available – there is an increased risk of intrapartum problems and fetal compromise
a. Caesarean section is often indicated, particularly if fetal monitoring shows fetal compromise,
malpresentation or if traumatic vaginal delivery is anticipated
b. Continuous CTG monitoring should be performed in all cases, and scalp pH or O2 saturation
should be checked if the CTG is non-reassuring (especially in recurrent IUGR pregnancy)
c. Cord blood gas testing is also useful – as many as 50% of IUGR infants have some degree
of metabolic acidosis requiring evaluation by the neonatology team
3. Following delivery:
a. Provide an environment as close to the intrauterine environment as possible – i.e.
temperature of at least 24°C or 26-32° if in an incubator. Supplemental O2 may be useful.
b. Prevent infection – avoid overcrowding, and ensure adequate hand-washing/hygiene
c. Adequate nourishment – start feeding 6hrs after birth, breast milk ASAP. Supplements may
be helpful e.g. Vitamin D, Vitamin C, niacin, riboflavin, Vitamin A.
d. Monitor for possible complications and treat as appropriate
Prognosis:
1. The rate of neonatal death, 5 minute Apgar <3, umbilical artery pH <7.0, seizures in the first day of
life and intubation are significantly increased in neonates born <3rd percentile birth weight
2. IUGR infants tend to remain physically small, though asymmetric infants may have accelerated
growth for the first 6 months of life (particularly if intrauterine deprivation was a major factor)

3. IUGR infants tend to have more neurologic and intellectual defects including lower IQ, learning and
behavioural problems
4. Others – increased risk of hypertension early in life, SIDS (IUGR infants account for ~30% of all
cases), Metabolic syndrome X (insulin resistance, loss of pancreatic β-cell mass, type II DM)
• Addendum: Ultrasound in O&G

Applications of ultrasound in pregnancy:
1. Maternal complications – ectopic pregnancy, threatened abortion, recurrent abortion (scan at 6-10
weeks), antepartum haemorrhage, co-existing disease (hypertension, diabetes, renal disease)
2. Fetal measurements – CRL, BPD, HC, AC and FL; fetal heart ± Doppler (in high-risk pregnancies)
a. Gestational age can be estimated reliably before 20 weeks as there is minimal variation from
the mean – CRL is measured from 6-12 weeks, BPD from 12 weeks and FL from 14 weeks
b. Fetal growth (size/weight) can be monitored by serial measurements – beware asymmetry
c. Fetal anatomy is abnormal in 3% of cases – 30-70% of significant structural anomalies can
be detected. ~80-90% elect for termination, otherwise more detailed scanning is indicated.
3. Placental measurements
a. Low placenta at 18-22 weeks (5% of women) suggests placenta praevia (5% of this group)
b. The placenta becomes more echogenically distinct near the end of the third trimester
4. Amniotic fluid volume – maximum vertical pool or amniotic fluid index
a. Oligohydramnios – reduced urine output, prolonged rupture of membranes, or severe IUGR.
Can lead to pulmonary hypoplasia, limb and facial deformities (Potter’s syndrome)
b. Polyhydramnios – maternal diabetes, gastrointestinal atresia in the fetus
5. Umbilical cord – single umbilical artery, nuchal displacement, cord presentation and vasa praevia
6. Invasive procedures – amniocentesis, chorionic villus sampling, cordocentesis, other procedures
Routine scans:
1. Early (11-14 weeks):
a. Estimate gestational age by measuring fetal crown-rump length
b. Diagnose multiple gestation and associated problems (e.g. twin-twin transfusion)
c. Screen for fetal chromosome abnormalities using nuchal translucency as a surrogate marker
d. Identify fetuses with gross structural abnormalities
2. Mid-pregnancy (18-22 weeks):
a. Estimate gestational age via BPD, HC, AC and FL
b. Detailed survey for structural abnormalities or markers of chromosomal abnormalities
c. Diagnose multiple gestation and associated problems if early scan not done
d. Locate the placenta and identify women with a low-lying placenta at risk of placenta praevia
e. Estimate the amniotic fluid volume
3. Other investigations:
a. Uterine artery Doppler – waveforms with a high resistance index or notch indicate poor
trophoblast invasion and indicate risk of pre-eclampsia, IUGR or abruptio placentae
b. Cervical length measurement (transvaginal scan) might identify risk of pre-term labour
c. 3D scanning can be done, but isn’t really useful except improving antenatal parental bonding
Routine scanning has been criticised as there does not appear to be any change in perinatal mortality, the
incidence of low birth weight or the overall neonatal condition. It is also costly and highly operator-dependent
– it is neither entirely sensitive or specific and problems that are missed or wrongly diagnosed can have
significant medical and medicolegal repercussions.
It is difficult to know how to counsel parents before their scan and full informed consent can be time-
consuming and in itself causes psychopathology. Similarly many chromosomal abnormalities picked up by
early scans will miscarry spontaneously, meaning the parents are overburdened unnecessarily by this
investigation.
At the end of the day, though, ultrasound is one of the safest tests ever – it is fairly well accepted that there is
no increased incidence of adverse effects on childhood cancer, dyslexia, speech development and other
variables. However, ultrasound is not completely non-invasive and can cause some localised effects (e.g.
heat) and newer machines use more focussed beams with a higher intensity than older scanners. Hence
exposure to ultrasound should be kept to the minimum required and only if indicated (if not a routine scan).
TUTORIAL 7: PRETERM LABOUR

“A 34-year-old P1G2 presents in labour at 31 weeks gestation with a breech presentation. Discuss.”

Key definitions:
• Labour – regular painful uterine contractions occurring greater than once every five minutes,
accompanied by a ‘show’ or by cervical dilation and/or effacement
• Preterm labour – labour occurring before 37 weeks gestation but not before 24 weeks gestation:
o Elective delivery e.g. for alloimmunisation or growth restriction
o Complicated emergency delivery e.g. placental abruption
o Uncomplicated spontaneous preterm delivery (30-40%)
o Preterm rupture of membranes
• Preterm Labour
Preterm labour is relatively common, with an incidence of between 5 and 10% in developed countries. It is
the foremost obstetric problem, accounting for 70% of neonatal morbidity and mortality. 75% are idiopathic,
10-20% are due to infection and the rest are due to uterine irritation. Risk factors include:
1. Maternal – age <18 or >35, poor nutritional state, tobacco (>20 cigarettes per day) or other
substance use, exercise (vigorous activity in third trimester), stress (corticotropin releasing factor)
2. O&G – previous preterm births, spontaneous early miscarriage, uterine abnormalities, uterine
distension, uterine distortion, compromised cervical structure, bacterial vaginosis, STDs and UTIs
Clinical features:
1. History – check dates; exclude other gastrointestinal or urogenital problems; beware haemorrhage
2. Symptoms – symptoms of labour i.e. increased uterine activity, early engagement of presenting part,
increased vaginal discharge or spotting, cervical effacement or dilatation
3. Signs – examine abdomen (exclude pathology) and uterus (soft and tender in chorioamnionitis,
tender lump in degenerating fibroid, tense and tender in placental abruption); check cervix
4. Investigations should include FBC + Kleihauer, U&Es, urine culture/microscopy, high vaginal and
endocervical swabs, ultrasound (diagnostic – assesses gestational age, growth, well-being)
Management:
1. Delaying labour for 48 hours allows time for steroids to mature the fetal lung. Contraindications
include fetal death, clinical chorioamnionitis, fetal/maternal condition requiring immediate delivery;
relative contraindications include vaginal bleeding, pre-eclampsia, fetal distress, IUGR and PROM
a. Nifedipine – Ca+2 channel blocker, inhibits myometrial contractions
b. β-agonists – reduces intracellular Ca+2, inhibits myometrial contractions
c. Magnesium sulfate – alters intracellular Ca+2 function, completely inhibits uterine contraction
d. Prostaglandin synthetase inhibitors – lowers PG peroxidase (stimulates uterine activity)
2. Improve fetal outcomes:
a. Corticosteroids to increase production and release of surfactant, with minimal risk to mother
(pulmonary oedema, infection, gastrointestinal haemorrhage)
b. Prevention of intraventricular haemorrhage – corticosteroids, phenobarbitone, vitamin K
3. Delivery:
a. Cephalic – vaginal delivery preferred with adequate analgesia; oxytocin best avoided
b. Breech – 26-32 weeks gestation benefit from caesarean section
• Preterm Rupture of Membranes

Preterm rupture of membranes has similar risk factors to preterm labour – in particular early pregnancy
bleeding (associated with infection or nutritional disturbance) and cigarette smoking. Aetiology varies but is
generally related to infection (Chlamydia trachomatis, group B Streptococcus, bacterial vaginosis).
Clinical features:
1. Symptoms – gush of fluid (distinguish from leaking urine), reduced fetal movements, contractions
2. Signs – flushed, increased temperature and pulse; oligohydramnios; pool of amniotic fluid in
posterior vagina on examination with speculum (also look for cervical dilation)
3. Investigations should include nitrazine stick (turns black in amniotic fluid), FBC, group and hold,
vaginal swabs (microscopy/culture/sensitivity), USS and CTG to assess fetal well-being
Management:
1. Antibiotic prophylaxis – chorioamnionitis in 25% of cases; use erythromycin and metronidazole
2. Preterm ROM <24/40 – generally poor outcome as there is no available therapy to replace or
maintain amniotic fluid
3. Preterm ROM 24-34/40 – viability is possible; delaying delivery is the treatment of choice in the
absence of infection or fetal distress. Steroids are given, aiming for delivery at 34-36/40
4. Preterm ROM >34/40 – survival is expected, consider active steps towards delivery at 36/40

TUTORIAL 8: FAILURE TO PROGRESS IN LABOUR
“A primigravid patient at 41 weeks is making poor progress in labour. Discuss likely causes and
management.”
• Physiology and Assessment of Normal Labour

Labour is defined as regular, coordinated contractile events of the uterus, leading to progressive cervical
dilation and subsequent delivery of products of conception. Contractions are typically 5 minutes apart
(increasing in frequency up to every 2-3 minutes), accompanied by a blood-stained or mucoid discharge
(show) or rupture of membranes, and cervical dilatation and/or effacement. Labour is divided into stages:
1. First stage lasts from the onset of regular painful contractions to full dilatation of the cervix
a. Latent (0 to 2-3cm) – cervical effacement, descent of the head
b. Acceleratory (2-3 to 10cm) – increased uterine activity, head descends and cervix dilates (at
least 1cm/hour for a primiparous; at least 1.5cm/hour for a multiparous)
c. Transition (10cm) – level of activity and progress reach a peak just before the second stage
2. Second stage lasts from full dilation of the cervix to delivery of the neonate
a. Flexion of the head Æ internal rotation of the occiput
b. Extension and birth of the head Æ restitution of the head
c. Birth of the anterior shoulder Æ birth of the shoulders and body
3. Third stage lasts from delivery of the neonate to delivery of the placenta
Nulliparous Multiparous
First stage 12 hours 8 hours
Second stage 2 hours 1 hour
Third stage 5-20 minutes 5-10 minutes
Assessment of labour involves plotting cervical dilation on a partogram (if plotted values lag behind the
expected dilatation by >2 hours, reassess and augment) and tracking descent of the presenting fetal part.
1. Maternal monitoring:
a. General well-being, pulse, blood pressure and respiratory rate every half an hour
b. Temperature and urinalysis for glucose, ketones and proteins every four hours
c. Abdominal exam – uterine contractions, descent of presenting part
d. Vaginal examination:
i. Cervix – effacement, consistency, dilatation, position (anterior/middle/posterior)
ii. Presenting part – nature, station, position, caput (cephalic oedema) and moulding
iii. Membranes and liquor
2. Fetal monitoring:
a. Liquor – meconium (2° to hypoxia) and blood (mild bleeding may be 2° to ‘show’)
b. Heart rate – should be 100-150bpm with >5bpm variability and no decelerations; continuous
monitoring (scalp electrode) should be done if there is increased risk of intrapartum hypoxia
c. Blood – acidosis reflects hypoxia; pH 7.3-7.4 normal but <7.2 needs emergency caesarean
• Prolonged Labour
Prolonged labour is defined as labour lasting more than 24 hours. It has numerous complications in both
the mother (low morale, exhaustion, dehydration, obstructed labour, uterine rupture, fever, amnionitis,
operative delivery, post-partum haemorrhage and endometritis) and fetus (infection, hypoxia and/or acidosis,
meconium aspiration, early rupture of membranes with cord prolapse, moulding, caput formation).
1. ‘Problems’:
a. Incorrect diagnosis of labour
b. Psychological (stress/mental exhaustion)
c. Failure of cervical dilatation due to previous trauma or repair Æ caesarean section
2. ‘Power’ (dysfunctional uterine activity):
a. Cervix does not dilate despite the presence of uterine contractions as these are hypotonic or
incoordinate. Common in primiparous women, may be related to low PGE2α levels.
b. Prevention by encouraging mobility, providing support and early fluids/analgesia; though
oxytocin may be needed (10U in 500mL fluids; aim for three 60s contractions in 10min)
3. ‘Passages’
a. Cephalo-pelvic disproportion is due to maternal pelvis disease (e.g. rickets), damage (e.g.
trauma) or deformity (e.g. orthopaedic disorders) or a large fetal head (e.g. hydrocephalus)
b. Good uterine contractions and head moulding will overcome minor disproportion, otherwise
caesarean section is required
4. ‘Passenger’

a. Malpresentation is the presence of any presenting part other than the vertex. Management
involves maximising the quality of uterine contractions and caesarean if irresolvable
i. Face (1:500) – fetal head fails to flex; landmarks are mouth, jaw, nose, bony ridges
ii. Brow (1:1500) – landmarks are anterior fontanelle and supraorbital ridges
iii. Breech (1:40) – extended (flexed at hips, extended at knees), fully flexed (hips and
knees both flexed) or footing (one or both thighs extended)
1. Risk factors – prematurity, fetal malformation, hydramnios, lax uterus,
pendulous abdomen, abnormal pelvic brim, placenta praevia
2. Diagnosis should be made antenatally and confirmed on USS; consider
caesarean section unless legs extended; consider external cephalic version
iv. Shoulder
v. Compound presentation – prolapse of a limb alongside presenting part
b. Malposition is the incorrect positioning of the vertex, most commonly occipito-posterior (10%
of all labours). Labour is usually prolonged in the first and second stage due to relative CPD
i. Diagnosis by abdominal exam (fetal head high, back and limbs easily felt) or vaginal
examination (early ROM, palpable anterior fontanelle, moulding or caput formation)
ii. 65% undergo long internal rotation (130°); 20% rotate partially (deep transverse
arrest) needing assistance; 15% remain and may be deliverable (but higher risks)
iii. Slow progress should be treated with titrated oxytocin infusion; if there is failure to
descend or concern about mother or fetus caesarean section is indicated
• Epidural Analgesia
Epidural anaesthesia can be done at T10-L1 for pain in late labour; T6-T8 for caesarean section or at S1
and below for delivery. BP and HR should be monitored every 5 minutes for at least 30 minutes.
1. Indications:
a. When requested by the mother – provides complete pain relief in 90% , decrease stress
(useful in women with symptomatic heart disease or vascular/hypertensive disorders)
b. Premature labour or incoordinate uterine activity
c. Fetoplacental dysfunction, breech presentation, multiple gestation
2. Contraindications:
a. Recent antepartum haemorrhage as compensatory reflexes are lost
b. Suspected cephalopelvic disproportion
c. Others – sepsis, allergy to local anaesthetic, anticoagulant therapy or coagulopathy
3. Complications:
a. The pushing reflex is abolished, though the ability to push is maintained if low doses used
b. Hypotension may compromise placental blood flow
c. Dural puncture headache may last 6-10 days if untreated
d. Others – neurological damage (motor paralysis), toxic reactions, aseptic meningitis
TUTORIAL 9: THE PUERPERIUM

“You have just delivered a 32-year-old of her third child (a normal delivery) and are called back to the
delivery room because she has very heavy vaginal bleeding. What do you do?”
“A 24-year-old G1P1 presents 6 days after a normal delivery at term. She feels feverish and unwell and has
a temperature of 39°C. Discuss diagnosis and treatment.”
• Physiology of the Puerperium

The puerperium is the time of recovery from pregnancy, labour and delivery. It usually last for 6 weeks, and
involves uterine involution, establishment of lactation and psychological adjustment to motherhood.
The uterus recedes from ~1000g to its pre-pregnancy weight (50-100g), mainly within the first 2 weeks in
response to oestrogen withdrawal (accelerated by oxytocin if breastfeeding). This is accompanied by lochia
(rubra Æ serosa Æ alba), a discharge consisting of blood and necrotic decidua; usually lasting 5 weeks.
The cervix also rapidly returns to its non-pregnant (though not nulliparous) state – the internal os closes by 3
days, while the external os closes by 3 weeks. Vaginal vascularity and oedema gradually resolves over 3
weeks, and the epithelium is restored by 6-10 weeks. Ovarian function varies depending on breastfeeding –
50-75% resume menses within 36 weeks if breastfeeding; otherwise mean time to menses is 7-9 weeks.
Lactogenesis is initially triggered by delivery of the placenta (unopposed prolactin action due to reduced
oestrogen and progesterone). Breastfeeding should be initiated as early as possible; feeding every 2-3
hours to stimulate milk production (should be well established by 36-96 hours). Colostrum is replaced by

milk after 3 days, at which point breasts are usually physiologically engorged. This can be alleviated with ice
packs, NSAIDs and by avoiding breast stimulation in women who elect not to breastfeed.
Other tissues – vulval swelling and engorgement is usually gone within 1-2 weeks, most perineal muscle
tone is regained within 6 weeks, and recovery of the abdominal wall depends largely on exercise.
• Post-Partum Haemorrhage
Post-partum haemorrhage is defined as excessive blood loss during or after the 3rd stage of labour. It may
be primary (occurring within 24 hours of delivery) or secondary (occurring 24 hours to 6 weeks post-delivery,
most frequently within 1-2 weeks).
1. Post-partum haemorrhage can be diagnosed objectively as a 10% change in PCV/Hct between
admission and the post-partum period; or transfusion requirement post-delivery 2° to blood loss
2. Normal blood loss is 450mL for vaginal delivery and 650mL for caesarean delivery, and post-partum
haemorrhage is usually diagnosed subjectively by relating actual blood loss to that expected
Incidence of primary post-partum haemorrhage is 4% in vaginal deliveries and 7% in caesarean deliveries;

while the incidence of secondary post-partum haemorrhage is 1-2% overall. Note that active management of
the 3rd stage of labour (prophylactic oxytocin, early cord-clamping/cutting, controlled cord traction, and
syntocinon infusion) dramatically reduces incidence of post-partum haemorrhage. Aetiology varies by type:
1. Primary post-partum haemorrhage:
a. Uterine atony (75-90%) leads to failed closure of spiral arteries and venous sinuses – risk
factors include uterine distension, rapid/long labour, amnionitis, muscle relaxants or oxytocin
b. Lower genital tract lacerations (10%) from obstetric trauma; more common with operative
vaginal deliveries (forceps/vacuum), macrosomia, precipitous delivery and episiotomy
c. Other causes include retained products of conception, uterine rupture, uterine inversion,
placenta accreta, coagulopathy/anaemia and haematoma
2. Secondary post-partum haemorrhage:
a. Causes include retained products of conception, infection (endometritis), subinvolution of the
placental site and coagulopathy
b. Management is conservative unless there are signs of infection, there is heavy bleeding, the
uterus is tender with an open os or there are retained products on USS (may Æ curettage)
Clinical features of primary post-partum haemorrhage:

1. Presentation – usually sudden onset of fainting, dizziness or distress with visible and/or intermittent
bleeding. There may be dramatic onset with pallor, sweating, loss of consciousness (i.e. shock)
2. History and examination:
a. Ask about parity, multiple gestation, polyhydramnios, previous post-partum haemorrhage,
history of bleeding disorders, desire for future fertility and oxytocin/MgSO4 use during labour
b. Inspect lower genital tract to identify lacerations and placenta to identify missing fragments;
bimanual exam may reveal retained placenta or haematoma of perineum or pelvis
3. Management:
a. Initial – O2, IV fluids, FBC, cross-match and coags; bimanual uterine massage, removal of
blood clots from uterus and catheterise, suture genital tract lacerations to improve view
b. Uterine atony:
i. Conservative – uterine massage, packing (can use large Foley), embolisation
ii. Ecbolic administration – syntocinon, ergometrine, or carboprost
iii. Surgery – bilateral uterine artery ligation, emergency hysterectomy
c. Other causes may require manual evacuation, dilation and curettage or hysterectomy
• Puerperal Pyrexia
Puerperal pyrexia is defined as a temperature >38°C for any 2 days out of the first 10 days after delivery
(except days 1 and 2). 90% will be due to urinary or genital tract infections, although other sites can be
infected e.g. breasts, chest and veins (thrombophlebitis). Predisposing factors include:
1. Antepartum – anaemia, poor nutrition, intercourse, premature rupture of membranes
2. Intrapartum – caesarean section, digital examination (>4), trauma, haemorrhage, prolonged labour
Endometritis is the main cause of post-partum infection; with an incidence of 2% in vaginal deliveries, 5-
15% in caesarean deliveries and up to 30-35% in patients who undergo caesarean following an extended
labour. Infection in days 1-2 is usually due to Group A Streptococci, days 3-4 usually due to E. coli or
anaerobes, post day 7 usually due to Chlamydia trachomatis and post-caesarean usually due to Bacteroides.
1. Risk factors – caesarean delivery, young maternal age, low socioeconomic status, prolonged labour,
premature rupture of membranes, multiple vaginal exams, intrauterine catheter, pre-existing infection
of lower genital tract and twin delivery

a. Fever, chills, lower abdominal pain, malodorous lochia, vaginal bleeding, anorexia/malaise
b. Fever >38°C, tachycardia and fundal tenderness, may be mucopurulent vaginal discharge
c. Investigations – FBC, blood cultures, urinalysis and culture, CXR if respiratory involvement
3. Management:
a. IV antibiotics until patient afebrile for 24 hours (>90% recover after 48-72 hours)
b. Uterine curettage only if there is evidence of retained tissue on USS
Urinary tract infections have an incidence of about 2%. Typical pathogens include E. coli, Group B
Streptococcus, Staphylococcus saprophyticus, Enterococcus faecalis and Proteus mirabilis.
1. Risk factors - caesarean section, forceps/vacuum delivery, tocolytic agents, induction of labour,
maternal renal disease, hypertension, epidural anaesthesia, catheterisation, prior UTI in pregnancy
a. Frequency, urgency, dysuria, haematuria, suprapubic/abdominal tenderness, no symptoms
b. Vital signs stable, patient usually afebrile with or without suprapubic tenderness
c. Investigations – urinalysis and culture, FBC
3. Management:
a. Empiric antibiotics for 3-7 days (norfloxacin unless breast feeding Æ use cotrimoxazole)
b. Catheterisation if bladder distended; remove after 24 hours and check for post-void residual
Mastitis has an incidence of 3%, usually 2° to milk stasis and cracked nipples. Staphylococcus aureus is
the most common cause (50%); other organisms include S. epidermidis, S. saprophyticus, Viridans
streptococcus and E. coli. Neglected, resistant or recurrent infection can lead to abscess (5-10% of cases).
a. Fever, chills, myalgia, warmth, swelling and breast tenderness
b. Investigations – none required, though USS might help
2. Management:
a. Conservative – moist heat, massage, fluids, rest, proper infant position during nursing
b. Antibiotics – flucloxacillin 250mg q6h, usually resolves within 48 hours
Other infections:
1. Wound infections may be perineal (incidence 1-10%) or abdominal (incidence 3-15%). Risk factors
include diabetes, hypertension, anaemia, steroids, chorioamnionitis, prolonged/premature labour
a. Clinical – erythematous, oedematous wound ± purulent discharge, haematoma, abscess
b. Management – analgesia, local anaesthetic spray, Sitz baths, abscess drainage, antibiotics
2. Thrombophlebitis may be superficial (incidence 1%, conservatively managed) or deep (requires
anticoagulation with IV heparin for 7-10 days and continued antibiotics)
3. Respiratory tract infections often occur due to atelectasis post-general anaesthetic. The most
common organism is Streptococcus pneumoniae, and antibiotics are used as required.
.
TUTORIAL 10: ABNORMAL UTERINE BLEEDING
“A 45-year-old woman presents with heavy periods. Discuss management.”
“Discuss your investigation and treatment of a 63-year-old woman who presents with a one-day history of
vaginal spotting.”
Key definitions:
• Abnormal uterine bleeding – changed frequency of menses, duration of flow or amount of bleeding
• Menorrhagia – prolonged (>7 days) and increased menstrual flow (>80mL per cycle) affecting life
• Metrorrhagia – variable amounts of intermenstrual bleeding
• Polymenorrhoea – bleeding occurring earlier than 21 days
9-30% of women of reproductive age suffer from menorrhagia. In NZ, 2-4% of women <50 years of age
consult their GPs each year with menstrual problems and these make up 11% of specialist referrals (making
up 25% of gynaecology outpatient clinic consultations). 1 in 5 women will have a hysterectomy by age 54, of
which 50% are done for heavy menstrual bleeding.
• Aetiology
Causes of menorrhagia include:
1. Dysfunctional uterine bleeding (50%) – no identifiable pathology but reflects a disturbance in normal
ovulatory function leading to abnormal stimulation of the endometrial lining
a. Ovulatory – more common, regular

b. Anovulatory – less common (extremes of reproductive age), irregular, can Æ iron deficiency
2. Inflammatory – infection, pelvic inflammatory disease
3. Neoplastic – adenomyosis, endometriosis, uterine fibroids, uterine hyperplasia/polyps, carcinoma
4. Metabolic – PCOS, functional ovarian tumours/cysts, persistent corpus luteum cyst, coagulopathy
5. Iatrogenic – incorrectly controlled hormone therapy (HRT/OCP), IUD, anticoagulants
Clinical features include:
1. History:
a. Symptoms – pain, bleeding (timing, frequency, volume), discharge, prolapse
b. Gynaecologic/obstetric history – LMP, previous menstrual period, sexual history, last smear
c. Other history – medical history, smoking, personal or family history of relevant conditions
2. Examination – inspect external genitalia, vagina and cervix; smear/swab, bimanual if age >20 years
3. Investigations:
a. Serum β-HCG to exclude pregnancy-related bleeding
b. General blood tests – FBC, iron studies, hormone profile, thyroid function
c. USS – endometrial hyperplasia (>12mm) or atrophy (<5mm), polyps, fibroids, ovarian cysts
d. Others – endometrial pipelle (rapid screening) to exclude endometrial carcinoma,
hysteroscopy (gold standard) for diagnosis of endometrial polyps, submucous fibroids
• Management
Medical management includes levonorgestrel IUD, tranexamic acid (menstruating days only), NSAIDs
(menstruating days only), high dose norethisterone (days 5 to 25), oral contraceptive pill (days 5 to 25) and
danazol (daily continuous, ↑adverse effects). Choice of agent depends on individual patient requirements:
1. Does the patient require contraception? – consider LNG-IUD, OCP
2. Does the patient have painful menstruation? – consider LNG-IUD, NSAIDs, OCP
3. Is the patient unable to tolerate hormone treatments – consider NSAIDs, tranexamic acid, LNG-IUD
4. Is the patient trying to conceive? – consider NSAIDs, tranexamic acid
Surgical management includes endometrial ablation (laser, diathermy or balloon) or hysterectomy

(vaginally, abdominally or laparoscopically). Generally ablation has shorter operating time, fewer
complications, faster recovery; while hysterectomy has greater patient satisfaction, improved quality of life
and greater improvement in symptoms.
• Postmenopausal Bleeding
Postmenopausal bleeding is defined as bleeding occurring later than 1 year following a woman’s last
menstrual period; alternatively bleeding occurring six months or more after menopause. Aetiology varies, but
in general carcinoma should be assumed until proven otherwise:
1. Vulva – carcinoma, urethral caruncle
2. Vagina – atrophic vaginitis (majority of cases), carcinoma, pessaries and other foreign bodies
3. Cervix – carcinoma of ectocervix, carcinoma of cervical canal polyp
4. Endometrium – carcinoma, sarcoma, mixed mesodermal tumours, hyperplasia, polyps, endometritis
5. Fallopian tube – carcinoma
6. Ovary – feminising tumours, granulosa cell tumour, theca cell tumour
Red flags during history and examination include:

1. Endometrial carcinoma – age, nulliparity, PCOS, obesity, unopposed oestrogen exposure,
tamoxifen, past cancer of breast, colon or ovary, smoking and diabetes mellitus
2. Cervical carcinoma – HPV, intercourse at an early age, multiple sexual partners, high risk partners
Investigations should include smears/swabs, ultrasound, pipelle sampling (96% sensitive) and/or
hysteroscopy dilatation and curettage (98% sensitive).
TUTORIAL 11: INFERTILITY

“A 24-year-old woman who is wanting to start a family comes to see you to seek advice. She has major
problems with obesity, hirsutism and irregular periods. What management would you consider?”
Key definitions:
• Fecundibility – the chance of pregnancy each month with regular unprotected intercourse (~20%)
• Subfertile – failure to conceive naturally within 2 years (will only conceive with assistance)
• Infertility – failure to conceive after 1 year of regular unprotected intercourse
o Primary infertility – have never conceived previously (~2/3 of cases)

o Secondary infertility – have conceived previously regardless of outcome (~1/3 of cases)
• Sterile – no possibility of pregnancy
• Infertility
Infertility has a prevalence of about 1/6 of couples attempting to conceive. 33% are due to male factors,
20% to anovulation, 15% to tubal factors, 10% to endometriosis, 5-10% to cervical factors; but 15% are
unexplained (including stress and environmental factors).
Clinical assessment of the infertile female:

1. Aetiology:
a. Anovulation – premature ovarian failure, PCOS, hypothalamic/pituitary insufficiency,
hyperprolactinaemia, metabolic disease (thyroid, renal, liver, underweight or obese)
b. Tubal factors – PID (1 episode Æ 10%, 3 episodes Æ 50%), previous ectopic pregnancy,
adhesions, endometriosis, peritoneal infections
c. Cervical factors – congenital, infection, post-surgery
2. History:
a. General – age, BMI, hair (hirsutism/alopecia), acne, previous surgery
b. O&G – menstrual history, past pregnancies/miscarriages, intercourse timing (in relation to
ovulation) and frequency (>2 times per month), contraception, gynaecologic history
c. Social – smoking, folate in diet
3. Examination:
a. General including BMI, blood pressure and temperature (increases 0.3°C post-ovulation)
b. Assess for endocrine/systemic disease (including PCOS)
c. Abdomen and PV exam (Spinnbarkeit mucus at mid-cycle)
4. Investigations:
a. Screen for hepatitis, rubella, Chlamydia and Gonorrhoea
b. Hormones – progesterone (mild luteal rise of >30 mmol/L in 3 cycles), LH (elevated days 2-
5), FSH, LH:FSH ratio (increased in PCOS), thyroid (hypothyroidism), prolactin
c. Ultrasound to visualise follicle development or change to secretory endometrium
d. Tubal patency testing with laparoscopy or hysterosalpingogram
Clinical assessment of the infertile male:

1. Aetiology:
a. Sperm – abnormal spermatogenesis (2° to mumps, orchitis, chromosomal abnormalities,
chemical/radiation exposure), oligospermia/azoospermia, abnormal morphology or motility
b. Anatomical – congenital, obstruction of vas deferens, varicocele (varicosities in spermatic
cord veins), 2° to infection (mumps, STIs, prostatitis), surgery or trauma
c. Endocrine – hyperprolactinaemia, hypothalamic or pituitary failure (tumour, radiation or
surgery), exogenous androgens, adrenal hyperplasia
d. Sexual dysfunction
2. History:
a. General – frequency of intercourse, difficulty with erection/ejaculation, pubertal development,
previous fatherhood previous STIs, surgery to genitourinary tract, exposure to heat
b. Social – smoking, EtOH, environmental toxins, illicit drug use
3. Examination:
a. 2° sexual characteristics
b. Genital examination particularly testicular volume
4. Investigations:
a. Semen analysis – volume >2mL, count >20x105/mL, motility >50%, viscosity, WBC, Abs
b. Blood tests – FSH (1° testicular failure, pituitary dysfunction), testosterone and LH
(androgen deficiency), karyotyping (exclude chromosomal abnormalities)
c. Others – swabs for Chlamydia and Gonorrhoea, post-coital test (>20 motile sperm/HPF)
Management obviously depends on the aetiology. General measures include timing of sexual intercourse
(every 2 days in the peri-ovulatory period i.e. days 12-16), education about ovulation
1. PCOS – weight loss, clomiphene citrate (anti-oestrogen)
2. Tubal disease – hysterosalpingogram, manual removal or balloon tuboplasty, IVF if severe
3. Endometriosis – laparoscopic ablation or excision effective for pain but not infertility Æ IVF
4. Male factors – intrauterine insemination (IUI), intracytoplasmic sperm injection (ICSI)
5. Idiopathic – empiric clomiphene, IVF, IUI, expectant
Assisted fertilization involves monitoring the menstrual cycle to time oocyte retrieval; incubating oocyte and
sperm in a test tube; and replacement of the resulting embryo in the uterus via the cervix. This procedure is

more efficient if HMG is used to stimulate follicle growth, and surplus embryos can be stored. Risks include
infection, bleeding and ovarian hyperstimulation syndrome (ovarian enlargement, blood hyperviscosity).
1. In vitro fertilisation – ovaries are stimulated and eggs are collected by transvaginal aspiration under
ultrasound guidance, fertilized and embryos returned to the uterus as an outpatient procedure
2. Gamete intrafallopian transfer – gametes are placed in the tubes via laparoscopic cannulation; used
if tubes are patent with a pregnancy rate of ~28% per cycle of treatment
3. Zygote intrafallopian transfer – cleaved embryo transfer can yield a higher pregnancy rate of 48%
4. Intracytoplasmic sperm injection – used in severe oligospermia; sperm taken from the epididymis or
testis in men with obstructive azoospermia (50% retrieval rate)
• Polycystic Ovarian Syndrome

Polycystic ovarian syndrome is defined pathophysiologically by increased insulin resistance, characterised
by a combination of anovulatory infertility, hirsutism, acne, menstrual disturbance (oligo- or amenorrhoea),
hyperandrogenaemia and enlarged ovaries on ultrasound with increased stromal thickening. 1 in 5 women
have polycystic ovaries, and 1 in 10 have PCOS – it is the most common cause of anovulatory infertility.
a. Symptoms include menstrual disturbance (44-58%), hyperandrogenism (hirsutism, acne,
alopecia), obesity (50%), infertility (46-80%) and recurrent miscarriage (2.5%)
b. Signs include increased BMI, acne, hirsutism, insulin resistance, hyperlipidaemia (xanthoma,
xanthelasma, arcus senilis) and increased blood pressure
2. Investigations:
a. Transvaginal ultrasound – enlarged ovaries with increased stromal density, pearl-necklace
appearance with peripheral follicles (~2.8mm diameter), endometrial thickness
b. Free testosterone
c. Other tests – androgens, 17 hydroxy-progesterone (no corpus luteum), LH and FSH on day
2-5 (ratio >3:1), prolactin, fasting insulin/lipid/glucose, TFTs and 24hr urinary free cortisol
3. Management:
a. Infertility – weight loss, clomiphene, IVF, metformin (insulin sensitising), laparoscopic drilling
b. Hirsutism – weight loss, OCP, cyproterone acetate, spironolactone, metformin
c. Obesity – weight loss, metformin
d. Menstrual irregularities – COC or POP for regular cycles
e. Prevention – weight loss, low cholesterol diet, smoking cessation, endometrial sampling
TUTORIAL 12: INCONTINENCE OF URINE

“A 39-year-old woman with two children complains of incontinence. What further questions would you ask
her and how would you manage this problem?”
Key definitions:
• Urinary incontinence – involuntary leakage of urine that represents a hygienic or social problem to
the affected individual
• Stress incontinence – involuntary loss of urine occurring spontaneously with increases of intra-
abdominal pressure in the absence of detrusor muscle contractions
• Urge incontinence – involuntary loss of urine occurring secondary to uninhibited bladder contractions
• Mixed incontinence – combination of stress and urge incontinence
Stress incontinence is characterised by small amounts of urine leakage occurring during stress (e.g.
laughing or coughing), generally worse during the day.
1. Aetiology:
a. Urethral hypermobility – pelvic floor weakness 2°to pudendal nerve damage from childbirth,
surgery, low oestrogen or ageing
b. Intrinsic sphincter deficiency – denervation of internal sphincter (less than 10% of cases)
2. Management:
a. Conservative:
i. Pelvic floor (Kegel) exercises promote hypertrophy and thickening of periurethral
muscle, tightening the pubococcygeal muscle. 50% improvement after 3-4 months.
ii. Electrical stimulation of the pudendal nerve via the rectum or vagina has a similar
mechanism of action and efficacy as Kegel exercises
iii. Vaginal pessary – mechanical support for bladder base, restores proximal urethra to
an intra-abdominal position
b. Medical:
i. Sympathomimetics to increase periurethral muscle tone – pseudoephridine or
imipramine leads to improvement in 50% of cases.

ii. Systemic/topical oestrogen is useful in menopausal women (may take 2-3 months)
c. Surgical (>85% cure rate):
i. Retropubic suspension – secures bladder neck and urethra to supporting structures
ii. Transvaginal suspensions – via perineum, useful if prolapse present
iii. Sling procedures – support at bladder neck, used in low urethral tone/pressure
Urge incontinence is characterised by episodic but frequent, sudden-onset imminent need to void; usually
with moderate to large amounts of urine.
1. Aetiology:
a. Detrusor dyssynergia (CNS abnormality) in 1% of cases
b. Idiopathic bladder instability (no CNS abnormality) in 99% of cases
2. Management:
a. Conservative – behavioural therapy aiming to regain cortical inhibitory control
i. Bladder drills are effective in 70% of patients but requires prolonged therapy
ii. Other options include biofeedback and hypnotherapy
b. Medical – 50-80% respond
i. Anticholinergics – oxybutynin, imipramine
ii. α-agonists
iii. Ca+2 channel blockers
c. Surgical – denervation has 50% cure, but can cause bladder hypotonicity (Æ catheterisation)
Other causes of incontinence include bypass incontinence (via fistulae, ectopic ureters or urethral
diverticulae), overflow incontinence (2° to retention), and functional incontinence (e.g. Alzheimer’s, disability).
• Uterovaginal Prolapse
Vaginal prolapse is described as a cystourethrocoele (anterior wall), rectocoele (posterior wall) or
enterocoele (posterior fornix); while uterine prolapse is classified as first-degree (cervix at ischial spines),
second-degree (cervix at introitus) and third-degree (cervix outside introitus).
1. Aetiology includes childbirth (pelvic floor damage), raided intraabdominal pressure (chronic cough,
constipation), and oestrogen deficiency (leading to reduced tone)
2. Symptoms are usually worse at night and include backache, difficulty with micturition or defaecation,
and dyspareunia. Bleeding and discharge may occur in procidentia (cervix outside vagina)
3. Examination:
a. Inspect introitus – separate labia while supporting anus with a swab, ask to bear down
b. View vaginal walls with a Sims speculum (ask to bear down to assess cervical descent)
c. Bimanual examination – uterine motility/descent, assess perineum and pelvic floor
d. Neurological examination – exclude multiple sclerosis or diabetic neuropathy
4. Management:
a. Prevention – repair of perineal trauma at delivery, pelvic floor exercises
b. Conservative – physiotherapy ± ring pessary
c. Medical – hormone replacement therapy
d. Surgical – vaginal hysterectomy and repair
TUTORIAL 13: ABNORMAL CERVICAL CYTOLOGY

“A 26-year-old woman was referred with a cervical smear result showing CIN-3 and HPV. Discuss
management.”
• Cervical Cancer
Human Papilloma Virus (HPV) is thought to be the main causative agent in the development of squamous
cell carcinoma of the cervix. It is usually sexually transmitted and most infections are silent – infection may
be detected decades after last sexual contact.
1. Biological behaviour – >80 serotypes of which 30-40 infect the human genital tract (of which only 3-4
produce clinical infection). Some serotypes become incorporated into epithelial cell DNA, and HPV
oncogenes (E6) bind to the tumour suppressor gene p53 (Li-Fraumeni syndrome increases risk 7x)
a. High oncogenic potential – HPV16, HPV18, HPV33 associated with subclinical infection and
low grade CIN which progresses to high grade CIN and invasive cancers
b. Low oncogenic potential – HPV6, HPV11 – associated with clinical and subclinical infection
and low-grade CIN, rarely invasive tumours.
2. Risk factors include early age of first coitus, frequent coitus with multiple sexual partners or a partner
with multiple sexual partners, smoking and low socio-economic status. Other possible risk factors
include partners of men with prostatic or penile cancer, divorce, other STIs, religious and cultural
factors, immunosuppression, hormonal contraception (barrier contraception is protective)

The transformation zone is the area between the original squamocolumnar junction and the current
squamocolumnar junction (i.e. the part of the cervix that was originally columnar epithelium and is now
squamous epithelium). This area undergoes squamous metaplasia (most actively during fetal development,
around the time or menarche and during pregnancy) and is importantly vulnerable to infection by HPV.
CIN 1 CIN 2 CIN 3

(Mild dysplasia) (Moderate dysplasia) (Severe dysplasia)
Well-differentiated epithelium Upper two thirds Upper half Upper third or absent
Nuclear abnormality Minor Moderate Marked, full thickness
Mitotic figures Few, basal third Basal two thirds, some Numerous, many
abnormal abnormalities
• Classification of Cervical Cytology

George Papanicolaou initially divided cervical cytology into five classes ranging from I (normal) to V
(carcinoma). This system was later modified, introducing the terms dysplasia (mild, moderate, severe) and
cervical intraepithelial neoplasia (grades 1-3). However, there was poor reproducibility between observers
and even between separate readings by the same observer – in addition, there was little correlation between
diagnostic categories and treatment options (e.g. 50% of CIN-1 regresses and <2% becomes cancer).
The Bethesda system was first used in 1991 and has standard throughout the world, replacing numerical
designations with a descriptive diagnosis of cellular change. Each report comprised three elements:
1. Adequacy – satisfactory, unsatisfactory or satisfactory but limited
2. General categorisation – within normal limits, benign cellular changes or epithelial cell abnormality
3. Descriptive diagnosis:
a. Benign cellular changes – due to infection or reactive changes not thought to be associated
with increased risk of developing CIN or invasive carcinoma
b. Atypical squamous cells of undetermined significance (ASCUS; specify favour reactive or
premalignant/malignant) – show cellular atypia but no clear signs of premalignant change
c. Squamous cell anomalies – low-grade squamous intraepithelial lesions (LSIL e.g. HPV and
CIN-1), high-grade squamous intraepithelial lesions (HSIL e.g. CIN-2, CIN3), invasive SCC
d. Glandular cell anomalies – atypical glandular cells of uncertain significance (AGUS; specify
favour reactive or premalignant/malignant), adenocarcinoma in situ, adenocarcinoma
• NZ Cervical Screening Policy

Regular screening should commence at age 20 years for all women who have ever been sexually active
(including lesbian woman). Screening should then be 3-yearly if results are normal (1 year if first smear or
previous smear >5 years ago; 6 months if limited; 3 months if unsatisfactory) and continue until age 70.
Women who have had a hysterectomy for a benign condition, with complete removal of a histologically
normal cervix and with a normal smear history do not need further screening. Women with a subtotal
hysterectomy still require 3-yearly smears. More frequent screening for women with risk factors for cervical
cancer (e.g. sexual behaviour, smoking, hormonal or contraceptive use) is not recommended as there is no
evidence that these women have a shorter pre-invasive period.
The Papanicolaou smear detects about 80% of all true cervical cancers with a false-negative rate of 20%
resulting mainly from sampling error. Retrospective data has shown that screening reduces the incidence of
cervical cancer by 60-80% and mortality by 90%. Colposcopy (using 3-5% acetic acid and Lugol’s iodine to
stain cells) with guided biopsy is the gold standard for diagnosis, with nearly 100% accuracy.
Lesion Progression and Follow-Up

1. ASCUS – majority do not persist in subsequent smears; 10-15% have persisting abnormalities; a
significant number show LSIL and a small number show HSIL.
a. If picked up with a normal smear history, next smear at 6 months (abnormal Æ colposcopy)
b. If either smear report specifically identifies possibility of HSIL, refer for colposcopy
2. AGUS – whether this is a precursor to adenocarcinoma in situ is controversial
a. “Favours reactive” with normal smear history, smear at 6 months (abnormal Æ colposcopy)
b. ‘Favours dysplasia’, refer for colposcopy after initial smear
3. LSIL (CIN1/HPV) – high regression rate (>50%), immediate colposcopy causes unnecessary anxiety
a. If no previous abnormality, smear at 6 months (abnormal Æ colposcopy)
b. Histology confirmed Æ management by observation (6-monthly smears, yearly colposcopy)
c. 3 consecutive normal smears (6 months, 1 year, 1 year) Æ back to 3-yearly screening
4. HSIL (CIN2, CIN3 – most progress to invasive carcinoma), adenocarcinoma in situ or carcinoma:

a. Refer directly for colposcopy
b. Histology confirmed Æ smear at 6 months, then yearly until the age of 70.
Treatment methods vary, but in general HSIL lesions should be treated within 2 months of histological
confirmation, and LSIL lesions should be treated within 6 months of deciding to treat (since they can be
managed conservatively with regular surveillance).
1. Excision:
a. LEEP/LLETZ – rapid, easily done, can be done under local anaesthetic but risk of scarring
b. Laser cone – expensive, more difficult to perform
c. Cold knife cone biopsy – requires general anaesthetic and risk of haemorrhage/scarring but
useful if whole lesion not visualised, past history of treated CIN, suspicion of AIS/malignancy
2. Ablation by cryocautery, laser, electrocoagulation or needle diathermy
a. Eliminates epithelium of the entire TZ (must be at least 5mm deep to destroy gland crypts)
b. Disadvantages – no histology for review, risk of inadequate treatment
TUTORIAL 14: CONTRACEPTION

“Doctor, what contraceptive is best for me?” “My family is complete and I wish to be sterilised.”
• Natural Methods
Fertility awareness (natural family planning, rhythm method) relies on abstinence during the times in the
menstrual cycle that could potentially result in pregnancy. Reliability ranges from 55-80% and often couples
report conflicts and frustration – there are also tenuous reports of fetal abnormalities due to aged gametes.
1. The beginning of the fertile phase can be recognised by
a. Calculation – subtract 21 days from the shortest cycle length (over the last 6 months)
b. Mucus (appears at the start of the fertile phase, peaks at ovulation – slippery/stretchy)
2. The end of the fertile phase is from the day after ovulation (day 12-16) which may be calculated via:
a. Temperature – 3/6 rule (temperature must be up for 3 days, above the previous 6 days)
b. Mucus – infertile on the 4th evening after the peak mucus day
Coitus interruptus involves withdrawal of he penis from the vagina prior to ejaculation. It requires a
significant amount of self-control from the male partner and has an effectiveness of 75-85%, due to sperm
that may be deposited in the vagina prior to orgasm and deposition of sperm near the introitus.
Lactational amenorrhoea occurs via hypothalamic suppression of ovulation. However, 50% of lactating
mothers begin ovulating after 6-12 months even while breastfeeding, and as a result 15-55% will become
pregnant. However, effectiveness can be as high as 98% if breast milk is the only form of nutrition for the
infant, and this method is only used for six months or when menses resume, whichever is sooner
• Barrier Methods
Condoms are latex sheaths (with or without a coating of lubricant or spermicide) placed over the erect penis,
physically preventing the passage of sperm into the vagina. To maximise effectiveness check expiry dates;
pinch the well at the tip before putting on; secure at base when withdrawing then check for tears; store in a
cool place and use only water-based lubricants (avoid vaginal thrush creams also).
1. Advantages – easily obtainable, cheap or free; highly effective if used correctly; protection against
most STDs; protection against cervical cancer; visible evidence of use; involves the male sharing the
responsibility; may increase the woman’s pleasure and minimised intercourse odours/messiness
2. Disadvantages – reduces spontaneity; decreased sensitivity; psychological barrier; allergy; messy,
distinctive odour; may slip/rupture (small leaks may Æ pregnancy); needs high degree of motivation
Diaphragms are rubber or latex domes that lie diagonally across the cervix, vaginal vault and much of the
anterior wall. It holds spermicide against the external os and provides a physical barrier, holding sperm
away from the alkaline cervical mucus long enough to die in the acidic vagina. It requires fitting, and must be
inserted prior to intercourse and left for 6-8 hours after.
1. Advantages – 80-85% effective if used properly; more independent of intercourse than condoms;
useful during menstruation; protection against most STIs but not viruses; may decrease risk of
cervical neoplasia and lasts around 5 years with good hygiene and cares
2. Disadvantages – involves forward planning (slight loss of spontaneity); some loss of cervical and
vaginal sensation; less effective than hormonal contraception or IUD; messy; local adverse effects
including increased risk of UTI, vaginal irritation, allergy, pressure effects, abrasions and ulcers
Spermicides (nonoxyol-9 and octoynol-9) come as foams, gels, creams and suppositories and act by both
killing sperm and by proving a mechanical barrier. They are 75-80% effective alone, but better when added

to condoms or diaphragms. They should be placed in the vagina at least 30 minutes before intercourse –
note that there is no protection against STIs.
• Intrauterine Devices
Copper-based intrauterine devices induce a spermicidal inflammatory response – they do not affect
ovulation. There are two types available – the Multiload Cu375s with a failure rate of 1 pregnancy per 100
women per year for at least 5 years; and the Nova-T which can be inserted into a smaller os but has a higher
failure rate of 2 pregnancies per 100 women per year for 3 years, after which risk increases further. They
may be inserted any time except day 1-5 (more likely to get expelled); or often 6 weeks after delivery.
1. Risks – doesn’t increase risk of PID but can worse current disease; reduce overall rate of ectopic
pregnancy but increased risk of ectopic pregnancy by 5x in those who do get pregnant; increases
rate of miscarriage and third trimester sepsis if left in during pregnancy; perforation rate of 1 in 1000
2. Contraindications – pregnancy; genital malignancy; undiagnosed genital tract bleeding; distorted
uterine cavity or cavity <5.5cm; Wilson’s disease; active gonococcal or chlamydial infection; pelvic
inflammatory disease; previous endocarditis or risks (e.g. anatomic heart lesion, prosthetic valve)
Hormone-based intrauterine devices is similar to a standard copper IUD but is covered in a sheath of
progesterone-secreting material. This inhibits sperm function, inhibits endometrial proliferation and alters
cervical mucus and has a success rate of 99.9%. Approximately 1/3 of women do not ovulate, and it is an
effective form of treatment for menorrhagia. Adverse effects usually are limited to the first three months and
include irregular bleeding, acne, abdominal cramps and breast tenderness.
• Hormonal Methods
The combined oral contraceptive pill provides contraception by inhibiting ovulation and by forming a
mucus plug in the cervix, with 99% efficacy if used correctly. The first pill is taken on the first day of menses,
and must be taken at the same time every day (±12 hrs) – contraception is not effective until 7 consecutive
hormone pills have been taken (except when the pill is started on day 1-3 of the cycle). The 7-day rule must
be re-applied if there is vomiting within 3 hrs, diarrhoea or if other medications are being taken (below).
1. Classification:
a. 2nd generation – ethinyloestradiol with levonorgestrel; ethinyloestradiol with norethisterone
b. 3rd generation – ethinyloestradiol with desogestrel; ethinyloestradiol with gestodene
c. Others – ethinyloestradiol with cyproterone acetate
a. Absolute – past or present circulatory disease, liver disease, history of serious disease
affected by sex hormones or related to previous OCP use, pregnancy, undiagnosed genital
tract bleeding, oestrogen dependent neoplasms and anxiety unrelieved by counselling
b. Relative (>1 relative = absolute) – positive family history but normal clotting factors, BMI of
30-39, limited mobility, extensive varicose veins
3. Advantages:
a. Simple, easy to use and don’t interfere with sexual intercourse
b. Improved menstrual cycle disorders; withdrawal bleeds usually regular, shorter, lighter and
less painful; anti-androgen pills (cyproterone) may help skin problems and PCOS symptoms
c. Small reduction in risk for endometrial cancer and ovarian cancer; reduced rates of
endometriosis, benign breast disease, benign ovarian cysts, PID and ectopic pregnancy
4. Disadvantages:
a. Adverse effects include weight gain, moodiness, skin changes, irregular bleeding and
nausea – there may also be nausea/vomiting, breast tenderness and bleeding on initiation
b. Amplifier of CVD and stroke risk factors, slightly increased risk of breast cancer and possible
weak co-factor for cervical cancer (promoter for HPV-induced carcinogenesis)
c. Increased risk of VTE – 1 per 30,000 baseline; 30 per 30,000 in pregnancy; 3 per 30,000 for
2nd generation; 6 per 30,000 for 3rd generation and 8 per 30,000 for cyproterone pills
5. Interactions and precautions:
a. Drugs – anticonvulsants, anti-TB drugs, antiretroviral drugs, griseofulvin (anti-fungal),
lansoprazole (PPI), tacrolimus (immune suppressant), St John’s Wort, grapefruit, antibiotics
b. Chronic illness – diabetes (POP preferable or 3rd generation pill – may raise insulin needs),
inflammatory bowel disease (may be aggravated), gallstones (increases presentation but not
incidence), epilepsy (higher dose required), migraine (use low doses), SLE (symptom flares)
The progesterone only pill acts by thickening cervical mucus (making it impenetrable to sperm) and alters
the endometrial lining to prevent implantation. 50% of women will ovulate normally, but up to 20% will not. It
must be taken at the same time every day (±3 hrs) but if taken correctly it is 97% effective. If taken on day 1-
3 it is effective immediately, otherwise it is not effective until 7 pills are taken (after which it is a 2-day rule).

1. Advantages – useful if oestrogen is contraindicated (sensitivity, breast feeding); no evidence of risk
in terms of circulatory or malignant disease; no effects on coagulation, BP, lipids or liver function
2. Disadvantages – adverse effects include irregular bleeding, breast tenderness and increased
functional ovarian cysts; higher risk of ectopic pregnancy in those who become pregnant (6% Vs 2%)
Depo Provera is an IM injection of 150mg medroxyprogesterone given every 90 days (more frequently if on
enzyme inducers). It reaches peak levels 24 hours after injection and acts by interfering with mid-cycle LH to
stop ovulation. Pituitary suppression causes endometrial atrophy so bleeding is irregular, heavy (20%) or
absent (60%). It is 99% effective immediately if given on days 1-3; otherwise the 7-day rule applies. After
the injections are stopped there is some delay in return of ovulation; fertility rates are normal by 18 months.
1. Advantages – useful if the combined oral contraceptive is contraindicated, epileptics, bowel disease
or sickle cell disease (reduces sickle cell crises); can be used post-partum and if breast-feeding
2. Disadvantages – adverse effects include weight gain, depression, reduced libido and vaginal
dryness; lowers bone density, probably no effect on breast cancer, protective for endometrial cancer
• Emergency Methods
Before prescribing an emergency contraceptive, it is important to determine present contraception,
unprotected sexual intercourse, dates of LMP, cycle length, current medications, coercion, STDs and plans
for future contraception. Opportunistic cervical screening and infection swabs may also be appropriate.
The emergency contraceptive pill may be either combined or progesterone-only (probably more effective)
– the former requires 2 pills to be taken within 72 hours of intercourse with another 2 pills taken 12 hours
later, while the latter only requires 1 pill per dose (note that those on enzyme inducing drugs may need a
double dose). It acts by delays the release of the ovum, and prevents hormone release from the corpus
luteum. Nausea is a common side effect (16%), though less common with levonorgestrel.
Another option is the postcoital IUD which can be inserted within 5 days of unprotected intercourse or
possible fertilisation. It prevents implantation of the fertilised ovum (interceptive) and is 100% effective –
however, if used after 5 days of ovulation it is liable to cause abortion.
• Sterilisation
Before undergoing sterilisation there are often a lot of long-term considerations to be made:
1. “Am I really happy with the size of my family?”
2. “What if I get a new partner and we want kids together?”
3. “What if something happens to our other children?”
Pre-sterilisation counselling (including consent) is mandatory and involves a full discussion of risks,
outcomes, effectiveness and finality of the decision. Factors associated with regret include young age, times
of stress, and operation immediately after delivery (i.e. puerperal sterilisation). Patients should be informed
that the procedure is not reversible (though in practise reversals may be successful)
Vasectomy involves ligation of the vas deferens, through a small incision in the upper outer scrotum under
local anaesthetic. Complications are rare but include bleeding, haematoma, skin infection and suture or
anaesthetic reactions. It is safer and less expensive than tubal ligation, though is not effective for 4-6 weeks
(when azoospermia is confirmed). Reanastomosis is successful in 60-70%, with pregnancy rates of 18-60%.
Tubal ligation is performed in hospital under general anaesthesia (interval sterilisation) or during Caesarean
section (puerperal sterilisation). The fallopian tubes are occluded with rights, ties, clips or segmental
excision, via laparoscopy or laparotomy. Complications are mainly those of anaesthesia, risk of damage to
other organs, internal bleeding and infection. It is effective immediately; reversal has a success rate of 50%.
TUTORIAL 15: THE CLIMACTERIC AND THE MENOPAUSE

“A 52-year-old woman with her LMP 6 months ago presents with hot flushes. Discuss management.”
Key definitions:
• Climacteric – the transitory period between reproductive capacity to nonreproductive state,
characterised by transient but progressive endocrine, somatic and psychologic changes
• Menopause – permanent cessation of menses (for at least 12 months) secondary to loss of ovarian
function; alternatively the final menstruation that occurs during the climacteric

There is an increasing proportion of women who have reached menopause and who live a third of their lives
with no ovarian function. The age of physiological menopause (typically 50-51) has not changed markedly
since antiquity and there are few factors that lower this age (smoking, hysterectomy, high altitude).
• Physiology of Menopause
Most oocytes are lost by atresia through life, with a critical decline in quantity and quality about 20-25 years
after menarche. Development of menopause is related to this – there are fewer oocytes, but also remaining
oocytes do not respond to gonadotropins. The premenopausal period is marked by:
1. Shorter menstrual cycle (short follicular phase) due to poor oocyte recruitment (fewer follicles)
2. Irregular vaginal bleeding due to intermittent secretion of oestradiol from residual follicles
Hormonal changes in menopause:

1. Androgens – androstenedione reduced 50%, testosterone mildly low (60% if oophorectomy),
DHEA/DHEAS reduced 60%/80%. Remainder from adrenals; normal functions include:
a. Some positive effects on bone mass (reduced Ca+2 excretion)
b. Possible detrimental effects on lipid/cholesterol metabolism
c. May increase insulin secretion (possibly via insulin resistance)
d. May play a role in enhancing stromal proliferation in breast cancer
2. Oestrogens – oestradiol markedly reduced, oestrone decreased to a lesser degree. Both from
adrenal, but mainly androstenedione Æ oestrone Æ oestradiol. Normal effects include:
a. Normal maturation and function of oocytes and certain uterine cells
b. Inhibition of osteoclast function (maintenance of bone density)
c. Increased triglycerides, reduced LDL and increased HDL cholesterol levels
d. Direct beneficial cardiac effects, possibly via inotropic activity and vasodilation
3. Progestins – progesterone levels low (only 30% of normal follicular phase levels), residual from
adrenals. Normal effects include establishment and maintenance of endometrial cycling.
4. Gonadotropins – both LH and FSH levels markedly elevated (FSH higher due to slower renal
clearance), 2° to low inhibin levels, which usually inhibits GnRH. Normal effects:
a. FSH – promotes follicular growth and induces LH receptor (regulated by inhibin)
b. LH – stimulates ovary (Graafian follicle) to produce oestradiol
Symptoms are basically a consequence of irregular ovarian function and oestrogen level fluctuation:
1. Early symptoms:
a. Hot flushes – affect 75% on a daily to weekly basis; 82% for >1 yr, and 25-50% for >5 yrs
i. Typically headache-like symptoms followed by a sensation of warmth with skin
flushing and perspiration ± palpitations, lasting ~4 minutes
ii. Probably due to vasomotor instability (abnormal transient vasodilation); there may
also be associated palpitations, night sweats and insomnia
b. Menstrual irregularity – usually the first clinical symptom of the climacteric
i. Generally a gradual decrease in both amount and duration, though this varies from
person to person (which may mask/reflect organic disease)
ii. Associated symptoms (mastodynia, abdominal bloating, oedema, headache and
cyclic emotional disturbances) also decline as oestrogen levels fall
c. Psychological symptoms include anxiety, irritability, dysphoria, dizziness and fatigue
2. Intermediate symptoms:
a. Atrophy of reproductive tract, breast and skin:
i. Oestrogen is the major growth factor of the female reproductive tract, so there are
varying degrees of atrophy of all the reproductive organs
ii. Low oestrogen levels are probably also responsible for generalised thinning and
loss of elasticity of skin. Body hair distribution may also be changed.
b. Incontinence – atrophy of supporting structures leads to stress incontinence, while urge
incontinence is due to autonomic instability and atrophic changes to bladder and urethra
3. Late symptoms:
a. Osteoporosis – oestrogen lowers osteoclast activity and raises osteoblast activity, and low
levels leads to mainly trabecular bone loss first seen in vertebrae and radius (c.f. senile
osteoporosis with cortical and trabecular loss seen first in the pelvic bones)
b. Cardiovascular disease – risk increases progressively until age 70 when it becomes equal to
that of men (prior to menopause, risk in women lags by roughly 10 years)
Diagnosis is clinical, with age as the most reliable risk factor (though 2° amenorrhoea should be excluded if
<40 years as only ~1% have entered menopause). Other laboratory tests (help confirm diagnosis) include:
1. FSH level >23 IU/L is ~65% sensitive and 79% specific (>40 IU/L specific but not sensitive)

2. Inhibin B level <30ng/L is ~46% sensitive and 78% specific
Differential diagnosis:
1. Amenorrhoea – weight loss, prolactinoma, PCOS, pregnancy
2. Vasomotor flushes – hyperthyroid, phaeochromocytoma, carcinoid syndrome, DM, chronic infection
3. Abnormal vaginal bleeding – endometrial polyps, hyperplasia, cancer
4. Vulvovaginitis – trichomoniasis, candidiasis, carcinoma
5. Osteoporosis – many, many, many conditions can result in pain mimicking vertebral compression
• Management
HRT is the replacement of oestrogen ± progesterone in women with physiological or artificial menopause
(e.g. 2° to oophorectomy or radiotherapy). As a result of recent research, HRT is no longer recommended
routinely in healthy post-menopausal women although final results will not be available until 2005.
1. HRT is only indicated for unmanageable menopausal symptoms in the absence of contraindications:
a. Absolute – pregnancy, unexplained vaginal bleeding, active/chronic liver disease, history of
endometrial cancer, history of breast cancer, recent thrombosis
b. Relative – high triglycerides, history of thromboembolic disease, gallbladder disease,
migraine headaches, uterine leiomyoma, seizure disorders
2. Available preparations:
a. Oestrogen-only – used only in women post-hysterectomy (raised risk endometrial cancer)
b. Oestrogen and progestogen – used in women with a uterus
i. Combined sequential: continuous oestrogen with 10-14d progestogen monthly, used
in perimenopausal women or those who have menstruated within 12 months.
ii. Combined continuous: combined oestrogen and progestogen, used in women who
have not menstruated for >1 year
3. Routes of administration:
a. Oral – easy to take, cheap and raises HDL but alters liver function and increases TGs
b. Transdermal – fewer adverse effects but more expensive, can get tachyphylaxis
c. Subcutaneous (6-monthly injection of oestradiol) – good compliance, but difficult to remove
d. Topical (vaginal) – useful for atrophic vaginitis (poor systemic levels)
4. Efficacy:
a. Improves menopausal symptoms, reduces osteoporosis (hip fractures reduced 5 per 10,000
person-years), reduces colorectal cancer (6 per 10,000), reduces Alzheimer’s disease (but
not short-term), reduces DM incidence in women with coronary artery disease
b. Increased cardiovascular risk (7 per 10,000), increased thromboembolic events (8 per
10,000), increased breast cancer risk (8 per 10,000), higher cholelithiasis and –cystitis risk
Other treatment options include:

1. Selective oestrogen receptor modulators (raloxifene) – useful with high risk of breast cancer; reduce
lipids and maintain bone but generally worsen hot flushes and still has venous thrombosis risk
2. Androgens – may improve sexual arousal and libido, but risk of liver effects and unproven long-term
3. Other medications that may be useful for hot flushes – venlafaxine 75mg od (serotonin and
noradrenaline reuptake inhibitor), gabapentin, clonidine 0.1mg/d (reduces tamoxifen-related flushing)
4. Alternative therapies have not been studied long-term and safety is of some concern:
a. Some efficacy seen with black cohosh and foods containing phyto-oestrogens
b. No efficacy proven with Dong quai, evening primrose oil, Vitamin E and acupuncture
TUTORIAL 16: GYNAECOLOGICAL MALIGNANCIES

“A 45-year-old woman presents with a central lower abdominal mass and epigastric discomfort. How will you
manage her?”
Cervical cancer is a leading cause of morbidity and mortality in developing countries – while screening has
reduced the mortality rate in developed countries, it is still the 8th most common cause of cancer mortality in
the USA. Nearly all cases are due to infection with human papilloma virus (i.e. cervical cancer is an STD) –
HPV 16 and 18 are found in 70% of cervical cancers, and HPV 31, 33 and 35 are found in 20%.
1. Risk factors include multiple sexual partners and early age of first coitus; others risks include male
partner with multiple partners, high parity, altered immune status, smoking and OCP (?promoter)
a. CIN-1 and CIN-2 are usually detected in women aged 24-27; CIN-3 in women aged 35+; and
cervical cancer in women aged 40-60 presenting with abnormal uterine bleeding (post-coital,
intermenstrual, postmenopausal)

b. Colposcopy may show a nodule or small ulcer that may bleed on contact (note that 5% of
normal women have benign cervical polyps), later progressing to a friable warty mass
c. Staging – stage I confined to the cervix; stage II beyond cervix but not to pelvic wall or lower
1/3 of vagina; stage III causes hydronephrosis or in pelvic wall or lower 1/3 of vagina; stage
IV extensive local infiltration or spread to distant sites
3. Management:
a. Depending on the extent of the lesion, options include laser therapy, cone excision,
cryosurgery and rarely Wertheim’s hysterectomy (uterus, paracervical tissue, pelvic nodes)
b. Radiotherapy and chemotherapy may be used as adjunctive therapy or as palliative therapy
to reduce bleeding/discharge/pain if the lesion has spread beyond the cervix
c. 5-year survival – stage I Æ 85%; stage II Æ 50%; stage III Æ 25%; stage IV Æ 5%
Uterine cancer includes a range of tumours (e.g. leiomyosarcoma, mixed mesodermal tumours) but the
most common is endometrial carcinoma. This is the most common gynaecological cancer, with an incidence
of 1.8 per 100,000 in women aged 15-44; 30.4 per 100,000 in women aged 45-64 and 48.6 per 100,000 in
women aged 65+ (incidence in this group is similar to ovarian cancer but twice that of cervical cancer).
1. Risk factors are related to unopposed oestrogen and include early menarche, late menopause,
nulliparity, HRT use, obesity (conversion of androstenedione to oestrone) Æ diabetes, hypertension.
Note that smoking interferes with hepatic conversion of oestrone to oestriol so actually lowers risk.
a. 75-80% present (usually early) with abnormal uterine bleeding, typically post-menopausal –
other causes in this group include polyps, endometrial hyperplasia and endometrial atrophy
b. While D&C is the gold standard, pipelle sampling is almost as good and less traumatic.
Endometrial thickness via USS is also useful (>12mm pre- and >4mm post-menopausal)
c. Staging – stage I confined to the uterus; stage II involving the endocervix or cervix; stage III
outside the uterus; stage IV outside the pelvis or invasion of the bladder or rectum
3. Management:
a. Treatment is by total abdominal hysterectomy and bilateral salpingooophorectomy with post-
operative radiotherapy (except in stage I disease where it doesn’t change overall survival)
b. 2° carcinoma is found in 17.5% of patients and must be excluded (commonly breast and
colon); recurrence should be monitored in both these and intra-pelvic sites (apex of vagina)
c. 5-year survival – stage I Æ 80-95%; stage II Æ 73%; stage III Æ 52%; stage IV Æ 27%
Ovarian cancer is neither common nor rare, with a lifetime risk of about 1 in 70 women. While incidence Is
similar to endometrial and cervical cancer, it has the highest mortality of all gynaecological malignancies as it
is usually silent until disease is advanced. Most are sporadic (although metastatic disease is not uncommon)
with <5% of affected women having a family history. 85% are epithelial, with the remainder consisting of
stromal and germ cell tumours (including dermoid cysts).
1. Aetiology is unknown – it is believed that dedifferentiation occurs in cells overlying the ovary, which
are then incorporated during ovulation. There is also genetic predisposition – baseline risk is 1.6%;
with family history this increases to 4-5% (1 first-degree relative) and 7% (>1 first degree relative)
a. Breast/ovarian cancer syndrome – autosomal dominant BRCA-1 gene mutation
b. Lynch II syndrome (HNPCC) – mutation in mismatch repair genes
2. Risk factors are related to frequency of ovulation so include early menarche, late menopause,
nulliparity and obesity. Protective factors include lactation, pregnancy, OCP use (5 yrs Æ ↓50% risk)
a. Most cases are asymptomatic and 2/3 have extrapelvic spread at diagnosis –symptoms
include bowel obstruction, urinary frequency/dysuria, heavy/irregular menses and ascites
b. Trans-vaginal USS and CA-125 level can aid diagnosis; CT and MRI usually don’t
c. Staging – stage I limited to ovaries; stage II involving one or both ovaries with peritoneal
extension; stage III peritoneal seeding; stage IV metastatic disease (distant sites)
4. Management:
a. Surgery is curative in early lesions, but as this rarely happens most treatment is palliative
using chemotherapy (cisplatin, carboplatin) and/or radiotherapy ± surgical debulking
b. 5-year survival – stage I Æ >90%; stage II Æ 70-80%; stage III Æ 20-30%; stage IV Æ 5%
MISCELLANEOUS CRAP FROM LECTURES

• Routine Antenatal Testing
Booking tests:
1. Full blood count (12 week values):
a. Hb 120g/L (± 7) 133g/L non-pregnant
b. Hct/PCV 0.35 (± 0.02) 0.394

c. MCV 86.2fL (± 3.6) 83.7fL
d. MCH 30.1pg 28.4pg
e. Platelets 275 x109/L 272-277 x109/L
f. WBC (total) 6 x10 /L (values up to 15 x109/L may be seen; up to 25 x109/L in labour –
9
note that lymphocyte and monocyte counts are usually unchanged)

2. Serology:
a. Syphilis screening - VDRL or EIA non-reactive
b. Rubella immunity (>11 IU/mL is satisfactory)
c. Hepatitis B – HBsAg negative; antibodies depend on vaccinations/exposure etc.
3. MSU:
a. Dipstick for protein and glucose should be negative
b. Culture negative, WBC <10/hpf, RBC <10/hpf
4. Blood group and antibody screen:
a. ABO and Rh groups
b. Antibody screen should be negative:
i. Associated with haemolytic disease – D, c, C, e, E; non-Rh include Kell, (k), Js, Fy
ii. Not associated with haemolytic disease – Lea, Leb, P
Vaginal examination and tests as indicated:

1. Cervical smear – opportunistic testing
2. Swabs – endocervical, high vaginal
Follow-up tests:
1. 28 weeks – FBC, Polycose (<7.8mmol/L), antibody screen if Rh negative
2. 36 weeks – FBC
• CTG Interpretation
Features on a CTG:
1. Baseline rate – normally 110-150bpm
a. Increased with prematurity, infection, maternal pyrexia, hypoxia
b. Decreased if post-term, heart block, hypoxia
2. Variability – normally 5-25bpm
a. Increased with high fetal activity states, acute or acute on chronic hypoxia
b. Decreased with fetal sleep (95% last <40 minutes), drugs, hypoxia
3. Accelerations – increase of at least 15 beats for at least 15 seconds. These are good.
4. Decelerations – no fixed definition. These are bad.
a. Early – 20-40bpm drop; mirror contractions; associated with head compression (not hypoxia)
b. Late – slight drop; mirror contractions but lag; associated with hypoxia
c. Variable (mild/moderate <60bpm drop for <60s or severe >60bpm drop for >60s) – most
common; steep-sided, variable in shape/timing; associated with umbilical cord compression
5. Contractions – too frequent or too prolonged contractions (>30mmHg) can reduce fetal O2 supply
• Labour
Labour is defined as painful regular contractions resulting in progressive dilatation and effacement (thinning)
of the cervix. It is normally a spontaneous process in a term pregnancy, with a single fetus in vertex
presentation after an uncomplicated pregnancy. This is followed by delivery of the fetus, placenta and
membranes with maternal effort.
Stages of labour
1. First stage – onset of labour until full dilatation (descent and engagement occur before this)
a. Latent phase (varies from 1-20 hours)
b. Active phase – regular intense contractions from 3-4cm dilatation
2. Second stage – full dilatation until delivery of the fetus; 1 hour in nulliparous, 30 min in multiparous
a. Uterine contractions become expulsive and the mother experiences the urge to bear down
b. The presenting vertex descends (LOA Æ internal rotation Æ OA) with some retraction at the
end of each contraction until the biparietal diameter reaches the introitus (crowning)
c. The fetal head is delivered (extension Æ restitution Æ external rotation) and the anterior
shoulder followed by the posterior shoulder, trunk and limbs
3. Third stage – delivery of placenta and membranes
a. Active management – oxytocic agent given with prompt clamping/cutting of the umbilical
cord, followed by controlled cord traction until placenta and membranes delivered completely
b. Physiologic management – baby is placed on breast or nipple stimulation performed

• Neonatal Resuscitation
Neonatal resuscitation is apparently very simple and often performed but often unnecessary though it is
generally successful. One thing to note is that while adults have cardiac arrests, neonates have respiratory
arrests. The first breath is important as it pushes fluids out from the alveoli and airways, establishing a
resting lung volume – this occurs in response to cord obstruction, cold air and physical discomfort.
Basic principles:
1. Prevent heat loss – radiant warmer, dry neonate, remove wet linen
2. Maintain open airway – head slightly extended (may use neck roll), suction of mouth and nose
3. Evaluate neonate:
a. A – position, suction, ET tube as necessary
b. B – tactile stimulation, PPV as necessary
c. C – chest compressions, medications as necessary
Asphyxia (progressive hypoxia with accumulation of CO2 and resultant acidosis) may be due to 1° apnoea
(rapid breathing with normal HR and BP) or 2° apnoea (irregular breathing with decreased HR Æ 2° apnoea
with decreased BP). Prompt resuscitation is important as any delay can increase difficulty and lead to brain
or other organ damage.
1. Assessment:
a. Respiratory effort – if apnoeic or gasping Æ PPV
b. HR <100bpm Æ PPV
c. Colour – if central cyanosis give supplemental O2
d. Meconium Æ suction mouth/pharynx/nose; if poor HR/respiration/tone more suction
2. Oxygen:
a. Free-flow O2 (at least 5L/min 100% O2 via mask, bag and mask or tubing) is used initially
with central cyanosis then withdrawn gradually – if cyanosis persists consider PPV.
b. Bag/mask ventilation (40-60 breaths/min at 30-40 then 15-20 cm H2O ) if apnoeic/gasping,
decreased HR or persistent cyanosis on 100% O2 (beware congenital diaphragmatic hernia)
c. HR should gradually respond – if not, assess chest movement and consider inadequate
seal, blocked airway or insufficient pressure
3. Reassess after 15-30s of ventilation by checking HR (stethoscope or umbilical/brachial pulse):
a. <60bpm – continue ventilation, start chest compressions (lower 1/3 sternum, 90/min)
b. 60-100bpm – if increasing, continue; if not increasing add chest compressions (if <80bpm)
c. >100bpm – watch for spontaneous respiration Æ stop ventilation
4. Intubate if prolonged PPV needed; bag/mask failure; diaphragmatic hernia or tracheal ?suctioning
Medications can be given via umbilical veins, peripheral veins or as endotracheal instillations:
1. Adrenaline (1-2mL/kg via ETT) – if HR <80bpm after PPV and chest compressions
2. Volume expanders (10mL/kg) – if signs of hypovolaemia
3. Bicarbonate (2mEq/kg; 4mL/kg over 2 minutes) – given in prolonged arrest
4. Naloxone (0.1mg/kg; 0.25mL/kg) – severe respiratory depression post-narcotic administration
• Nutrition and Breastfeeding

Nutrition regulates growth. The fetal supply chain is probably useful here – maternal circulation Æ uterine
flow Æ placental transport Æ umbilical flow Æ fetal circulation Æ tissue uptake). A number of things can go
wrong at various points of this supply chain that can lead to a small or large-for-dates fetus. I’m not entirely
sure why I wrote this down in the lecture, as the rest seems to deal with nutrition in the neonate.
Daily requirements:
1. Fluids – 4mL/kg/hr (up to 10kg) + 2mL/kg/hr (10-20kg) + 1mL/kg/hr (>20kg). Note that neonates are
born with 10% extra fluid volume by weight, which is typically lost within the first three days of life)
2. Aim for 50% carbohydrates, rest fat and protein:
a. Carbohydrates – 11-14g/kg/d for first 3 months
b. Fat – 5-7 g/kg/d
c. Protein – 2-2.5g/kg/d
3. Minerals:
a. Na+ - 3-4mmol/kg/d
b. K+ - 2-3mmoll/kg/d
c. Ca+2 – 1mmol/kg/d

Lactogenesis is the initiation of milk secretion, which begins immediately after delivery in response to a
sudden decline in oestrogen levels (which until this point inhibits milk secretion). Suckling (which is in
proportion to infant appetite) leads to secretion of prolactin and oxytocin:
1. Prolactin (anterior pituitary) stimulates the epithelial alveolar cells to produce milk. It is controlled by
two hypothalamic regulators (prolactin releasing factor and prolactin inhibitory factor. Stress, general
anaesthesia, surgery, hypoglycaemia, oestrogens and retained products can inhibit prolactin release
2. Oxytocin (posterior pituitary) causes myoepithelial cells to contract leading to milk ejection. It is
released in response to suckling, tactile stimulation or even by Pavlovian association. Oxytocin may
be blocked by stimuli that increase adrenaline and noradrenaline (leading to relative ischaemia)
3. Growth hormone (similar structure to prolactin) also increases milk production mainly by increasing
substrates available. It also increases BP3 (binding protein for IgF) and mammary blood flow.
Breast milk is good. Note that severely premature infants may not be capable of suckling – this reflex
develops at 30-32 weeks, and by 35 weeks most neonates should be capable of suckling. Breast feeding
should be continued until the infant is weaned. This should occur when the infant can sit upright with
support, and can reach out and take foods; usually at 4-6 months of age (teeth appear at 5-10 months).
1. Benefits:
a. Anti-infection properties – IgG, IgA, complement, T and B-cells, lactoferrin (binds iron
making it unavailable for viral or bacterial use in the gut) and B12 binding factor (similar)
b. Supplies larger amounts of antigenic material Æ greater resistance, reduces risk of eczema,
wheezing, food allergy
c. Reduces risk of sudden infant death syndrome, necrotising enterocolitis, premenopausal
breast cancer, maternal osteoporosis, mastitis and engorgement
d. Contraceptive – as effective as the pill (though more effective in under-developed countries)
a. Medications – chemotherapy, antipsychotics, neuroleptics, bromocriptine, ergotamine
b. HIV – 15% risk of infection if all other factors controlled for; however benefits may outweigh
risks in underdeveloped countries where infectious diseases and malnutrition are important
c. Hepatitis C – relative contraindication, though care should be taken to avoid direct blood
contact (e.g. nipple trauma). Note that there is 1-5% risk of carriage in household contracts.
d. Not contraindicated in maternal HSV, rubella (encouraged – protective), CMV (protective),
hepatitis B (if infant and mother both given vaccine and immunoglobulin) and chickenpox.\
3. Alternatives:
a. Cow’s milk – poorer iron absorption (10% c.f. 50% from breast milk)
b. Goat’s milk – similar to human milk and easier to digest than cow’s milk (whey vs. casein)
c. Soy milk - ? oestrogenising effects so not first choice
d. Hydrolysed proteins – easily digested
Engorgement occurs when inefficient milk removal combined with increased blood flow to the breasts
creates lymphoedema. This limits milk outflow, leading to accumulation of suppressor peptides and
decreasing milk secretion. It is abnormal, and may follow-on from mismanagement of the normal state of
transient breast fullness following parturition. Management should aim to reduce distension so breastfeeding
can resume – this includes hand expression, breast pumping, hot and cold packs and analgesia.
Mastitis is inflammation in the breast producing localised tenderness, erythema, heat, swelling and systemic
reactions (including fever, malaise, shivering and acute flu-like symptoms). Often a lump can be found
localised to one of the lobes, indicating a blocked duct. It is more common in primipara than multipara and
tends to recur. The organism is usually Staphylococcus or E. coli (uncommonly Streptococcus) – note that
breast milk is not infected so there are no effects on the infant.
1. Classification:
a. Non-infective – inflammatory reaction following milk leakage into the surrounding tissue
b. Infective:
i. Cellulitis of the interlobular connective tissue – pus rarely found
ii. Adenitis (infection within the ductal system) – pus may appear in the milk
2. Aetiology:
a. Nipple trauma 2° to poor positioning of the baby is associated with early incidence
b. Oversupply in the early weeks while the milk supply is adjusting to the infant’s needs
c. Failure to empty breast, engorgement, infrequent or irregular breastfeeds in the early weeks
or when weaning; inappropriate use of bottles
3. Management:
a. Empty the breast – correct breastfeeding, hot and cold packs
b. Antibiotics if symptoms last >12-24 hours (flucloxacillin or cephalosporin for 10 days)
c. Surgical drainage if breast lump unable to be emptied by breastfeeding or expressing


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“I hate” Obstetrics and Gynaecology

TUTORIAL 1: RISK ASSESSMENT IN OBSTETRICS

• Maternal Risk Assessment

© Kevin Luong 2003 1

TUTORIAL 2: EARLY PREGNANCY PROBLEMS

• Bleeding in Early Pregnancy

Clinical approach to early pregnancy bleeding:

2 © Kevin Luong 2003

© Kevin Luong 2003 3

TUTORIAL 3: HYPERTENSION IN PREGNANCY

Hypertension in pregnancy is a common complication of pregnancy, occurring spontaneously in 8-10% with

4 © Kevin Luong 2003

© Kevin Luong 2003 5

• Glucose Metabolism in Pregnancy

Complications of diabetes mellitus in pregnancy include:

• Screening Tests for Gestational Diabetes

6 © Kevin Luong 2003

Antenatal management should be coordinated in a specialist multidisciplinary clinic, involving an

TUTORIAL 5: ANTEPARTUM HAEMORRHAGE

© Kevin Luong 2003 7

• Other Causes of Antepartum Bleeding

8 © Kevin Luong 2003

• Aetiology and Complications

• Assessment and Investigations

© Kevin Luong 2003 9

• Management and Prognosis

10 © Kevin Luong 2003

• Addendum: Ultrasound in O&G

TUTORIAL 7: PRETERM LABOUR

© Kevin Luong 2003 11

• Preterm Rupture of Membranes

12 © Kevin Luong 2003

• Physiology and Assessment of Normal Labour

© Kevin Luong 2003 13

TUTORIAL 9: THE PUERPERIUM

• Physiology of the Puerperium

14 © Kevin Luong 2003

Incidence of primary post-partum haemorrhage is 4% in vaginal deliveries and 7% in caesarean deliveries;

Clinical features of primary post-partum haemorrhage:

© Kevin Luong 2003 15

16 © Kevin Luong 2003

Surgical management includes endometrial ablation (laser, diathermy or balloon) or hysterectomy

Red flags during history and examination include:

TUTORIAL 11: INFERTILITY

© Kevin Luong 2003 17

Clinical assessment of the infertile female:

Clinical assessment of the infertile male:

18 © Kevin Luong 2003

• Polycystic Ovarian Syndrome

TUTORIAL 12: INCONTINENCE OF URINE

© Kevin Luong 2003 19

TUTORIAL 13: ABNORMAL CERVICAL CYTOLOGY

20 © Kevin Luong 2003

CIN 1 CIN 2 CIN 3

• Classification of Cervical Cytology

• NZ Cervical Screening Policy

Lesion Progression and Follow-Up

© Kevin Luong 2003 21

TUTORIAL 14: CONTRACEPTION