Normal pregnancy ........................................................................................................... 3
ANATOMICAL / PHYSIOLOGICAL CHANGES / SYMPTOMS ............................................ 3
ANTENATAL PATHWAY / SCREENING.............................................................................. 6
ANTENATAL COUNSELLING .............................................................................................. 8
CLINICAL............................................................................................................................ 10
Factors affecting embryo and fetal development ....................................................... 11
Obstetric history.............................................................................................................. 11
Adverse effects of exogenous hormones, drugs, irradiation and infectious conditions .. 12
Application, risks and information derived from use of CVS, amniocentesis, XR and
ultrasound....................................................................................................................... 17
Signs during pregnancy indicating fetal malformation .................................................... 19
Formation, constitution and significance of amniotic fluid .............................................. 19
Abnormal pregnancy ..................................................................................................... 22
ANTEPARTUM HAEMORRHAGE...................................................................................... 22
INTRAUTERINE MONITORING / GROWTH RESTRICTION ............................................ 25
PRETERM LABOUR........................................................................................................... 27
MEDICAL COMPLICATIONS IN PREGNANCY (HTN, DM, UTI…) ................................... 29
Labour............................................................................................................................. 38
Abnormal labour ............................................................................................................ 48
IDENTIFYING AN ABNORMAL LABOUR .......................................................................... 48
TWIN PREGNANCY ........................................................................................................... 48
ABNORMAL / ASSISTED DELIVERY ................................................................................ 49
POSTPARTUM HAEMORRHAGE AND SHOCK ............................................................... 53
Problems in early pregnancy........................................................................................ 56
Miscarriage (types and how to differentiate one from the other) .................................... 56
Early pregnancy loss (major causes, steps in management) ......................................... 56
Mid-trimester pregnancy loss (possible causes, discuss their management) ................ 57
Cervical incompetence ................................................................................................... 57
Examine pregnant patient bleeding in 1 trimester and make diagnosis ....................... 58
History from a patient with previous miscarriage and discuss likely causes .................. 58
Lower abdominal pain (differentiating signs and symptoms) ......................................... 59
Termination of pregnancy (ethical and medicolegal issues) .......................................... 59
Trophoblastic disease (Dx and Rx) ................................................................................ 59
Ectopic pregnancy (aetiology, pathology and Rx) .......................................................... 60
The pueperium ............................................................................................................... 62
ADJUSTMENT TO BABY ................................................................................................... 62
ABNORMAL PUERPERIUM............................................................................................... 64
Infertility.......................................................................................................................... 65
Structure and function of human reproductive organs ................................................... 65
Physiology of menstrual cycle ........................................................................................ 66
Actions of female sex hormones .................................................................................... 66
Factors necessary for fertilisation and implantation ....................................................... 67
Contraception and relative efficacy ................................................................................ 67
Sterilisation and medico-legal aspects ........................................................................... 72
Counselling individual/ couple in contraceptive techniques ........................................... 73
Counselling woman with pregnancy following contraceptive failure............................... 74
Investigation of infertile couple ....................................................................................... 74
Factors influencing human fertility (incl. psychological/ emotional sequelae) ................ 77
Management of common causes of infertility ................................................................. 77
Ethical implications of new reproductive technologies ................................................... 77
Ethical issues of contraception including sterilisation..................................................... 77
Genital tract infections .................................................................................................. 78
Reproductive endocrinology ...................................................................................... 82
Elicit, present and discuss the history of a patient with gynaecological disorders ......... 82
Recognise normal physical signs on pelvic examination ............................................... 82
Abnormal vaginal bleeding (investigations and management) ....................................... 82
Cameron Korb-Wells & Kai Brown (2009)
Dysfunctional uterine bleeding (diagnosis and management)........................................ 83
Postmenopausal bleeding .............................................................................................. 84
Amenorrhoea.................................................................................................................. 85
Oligo-amenorrhoea / PCOS (cause and management) ................................................. 87
Hirsuitism/ severe acne (investigations and management) ............................................ 89
Menopause management (risks and benefits of HRT) ................................................... 89
Premenstrual Syndrome (management) ........................................................................ 89
Dysmenorrhoea .............................................................................................................. 90
Chronic pelvic pain without pelvic pathology (causes and management) ...................... 92
11 The pelvic floor and urinary incontinence ........................................................... 95
PELVIC ANATOMY ............................................................................................................ 95
UTEROVAGINAL PROLAPSE ........................................................................................... 96
URINARY INCONTINENCE ............................................................................................. 100
Gynaecological cancers............................................................................................ 102
Aetiology and preventative factors in reproductive system malignancy ....................... 102
Cervical smear and knowledge of other techniques to diagnose malignant and premalignant lesions of the female reproductive system................................................... 108
Management strategies of malignant lesions of the female reproductive system ........ 110
Prognosis of common malignant neoplasm of the female reproductive system .......... 111
Counselling of a patient with a malignant lesion of the reproductive system ............... 111
Cameron Korb-Wells & Kai Brown (2009)
1. Discuss the changes in female anatomy occurring during a normal pregnancy.
2. Discuss the symptoms that are presumptive of early pregnancy.
5. Discuss the origin and the effects of the endogenous hormones, (oestrogen,
progesterone, human placental lactogen, oxytocin, prostaglandins, chorionic
gonadotrophin) during pregnancy.
10. Discuss physiological and emotional changes that may occur in pregnancy,
including postnatal depression.
15. Demonstrate a working knowledge of the immunological changes that are
associated with pregnancy.
 Amenorrhoea
 N/V
 Breast tenderness
 Urinary frequency
 Fatigue
Softening of the cervix (Goodell’s Signs) – 4-6 weeks
Bluish discolouration of the cervix and vagina (Chadwick’s sign) – 6 weeks
Uterine enlargement
Softening of the isthmus (Hegar’s Sign) – 6-8 weeks
 ßhCG
o positive in the serum at 9 days post-conception
o positive in the urine 28 days after LMP (last menstrual period)
transvaginal U/S
o 5 weeks: gestational sac visible (ßhCG = 1,200-1,500 mIU/mL)
o 6 weeks: fetal pole seen
o 7-8 weeks: fetal heart tones visible
transabdominal U/S
o 6-8 weeks: intrauterine pregnancy visible (ßhCG = 6,500 mIU/mL)
Physiological Changes in Pregnancy
progesterone induces relaxation of smooth muscle, among other effects
physiologic changes are more pronounced in multiple gestations
 ↓ BP – slowly increases towards term
 Plasma volume ↑ 50%
 TPR ↓ 30%
 CO ↑ 50%
o May have SEM due to hyperdynamic circulation
 ↑ blood flow to ureters, kidneys, uterus, breasts, skin.
Cameron Korb-Wells & Kai Brown (2009)
Enlarging uterus compresses IVC and pelvic veins ↑ risk varicose veins,
haemorrhoids and oedema.
 TLC, RV ↓
 Tidal volume and minute ventilation ↑ 50%
o ↑ TV causes respir. Alkalosis (↓ PaCO2 to 35mmHg and pH to 7.45)
o Compensated by ↑ renal bicarb loss
 ↑ GOR
o Lower LOS tone, delayed gastric emptying, ↑ abdo pressure
 ↓ motility in GIT
o Constipation
o Stasis in gallbladder (↑ risk stones)
 Upwards displacement of appendix (may have atypical presentation)
 Haemorrhoids
 ↑ GFR 50%
o ↑ Urate + CrCl but same UO as ↑ reabsorption
o Physiologic glycosuria (saturates reabsorption capacity)
 Urinary frequency
 Physiological dilatation of ureters (progesterone effect
o R > L due to uterine enlargement
 ↑ risk of UTI and pyelonephritis
 Striae gravidarum – stretch marks (fade but seldom disappear)
 Spider angioma and palmar erythema - ↑ oestrogen
 Chadwick sign – bluish colouration of vagina/cervix
 Linea nigra – increase in pigmentation from pubis to umbilicus in midline
 Cholasma – blotchy pigmentation of nose and face
 Oestrogen – promotes growth of ducts
 Progesterone – alveoli enlarge
 Prolactin – induces formation of proteins and lipids
 Oxytocin – induces SM contraction and lactation
 ↑ plasma vol > Hct = dilutional anaemia
 ↑ risk DVT and PE
o Oestrogen state
 ↑ coag factors
 ↓ anti-coag factors
o Venous stasis
 ↑ WBC (but impaired function)
o WBC 12 can be normal, up to 25 in labour/postpartum
o Often there is an improvement in autoimmune conditions
 Thrombocytopenia
o ? due to accel. Plt consumption
o Count normalises within 2-12 weeks post-partum
 Oestrogen ↑
o Estradiol
o Maternal, placental, foetal contributions
o Sudden ↓ may indicate foetal compromise
 Progesterone ↑
o Corpus leuteum in first 7/52, then placenta
o Maintains endometrium
 Human chorionic gonadotrophin
o Placental trophoblast
o 2 subunits – alpha (common to LH, FSH and TSH) and beta
 maintains corpus luteum
Cameron Korb-Wells & Kai Brown (2009)
b-HCG +ve 8-9 days post-ovulation
Levels double every 1-2 days, peak at 10 wks then fall to plateau
at term
 Rule of 10’s
• 10 IU at missed menses
• 100,000 IU at 10 wks (peak)
• 10,000 IU at term
 Low levels suggest ectopic, abortion or wring dates
 High levels suggest multiple gestation, molar pregnancy,
trisomy 21 or wrong dates.
Moderate enlargement and ↑ BMR
↑ total T4 (free T4 and TSH normal as TBG also ↑)
o Cortisol ↑
o Produced by corpus luteum/ovary
o Relaxes symphysis pubis and pelvic joints
o Helps soften and dilate cervix
o Inhibits uterine contraction
Ca Metabolism
o ↓ albumin = ↓ total Ca
o Free Ca stays normal (↑PTH)
 No bone path as PTH counteracted by ↑ oestrogen.
a) Maternity "blues"
b) Antenatal and Post-natal depression (PND)
c) Post-partum psychosis
Childbirth & Becoming a Parent requires the capacity for rapid & massive
psychological adjustment
Maternity ‘blues’
• A benign condition: 50-60%.
• Sx peak b/n 3rd-5th day and gone by 10th day.
• Mood lability: elation (days 1-2), irritability, anxiety, depressed, poor concentration.
• Up to 30% go on to subsequent PND (severe cases)
• Treatment: reassure but be aware it may be early stages of PND
Cameron Korb-Wells & Kai Brown (2009)
4. Understand the problems that may arise in determining the time of conception if the
patient is not certain about the date of her last menstrual period.
6. Discuss investigations and tests that are used to assess fetal wellbeing.
8. Discuss the relevance of screening antenatal investigations, including ultrasound.
Estimating Dates
 Conception – 38 weeks from conception
 LMP – 40 weeks from LMP
o Assumes 28 day cycle (normal cycle can vary 21-35 days)
 Luteal phase always 2/52, proliferative phase variable.
o Only 10% of women have 28 day cycle
o Naegele’s rule – LMP – 3mo + 7days
 U/S dating
o Most accurate in 1 Trimester (8-12wks), as baby grows variations in
size do not correlate to gestational age as well.
o Only take US date if more than 1 week discrepancy to LMP dates.
Trimesters – normal pregnancy term: 37 to 42 weeks
 T1 (first trimester): 0 to 12 weeks
o N/V, breast tenderness, frequency
o Spotting 20% (50% will continue as per normal)
o Complications – spontaneous abortion
 T2 (second trimester): 12 to 28 weeks
o Generally no AE ± round ligament pain
o Braxton-hicks (painless, low-intensity, long) from >14wks
o Fetal movement (quickening) from 18-20wks
o Complications – incompetent cervix, PROM, premature labor
 T3 (third trimester): 28 to 40 weeks
o ↓ libido, back pain, leg pain, frequency, constipation
o Decent into pelvis (“Lightening”) – eases maternal breathing
o Bloody show – mucous plug passage
o Complications – PROM, premature labor, pre-eclampsia, GDM, UTI,
Antenatal Timeline
Each visit ask re: problems, bleeding, pain, preg. Symptoms, measure fundal height, weight
~q monthly to 28wks, then ~q 2wks to 36wks, then q weekly to term.
Antenatal Care
O&G Hx, Med Hx
Diet weight
Advise re: ETOH,
smoking, meds/drugs,
testing, folate/Fe,
travelling to endemic
Rubella Titre
Pap Smear
At booking (~8wks)
As above
Estimate dates by LMP
Blood Group
Syphilis serology
HIV, rubella, HepC ± STD
? consider dating
US 8-12 weeks
b/g risk – major 1%,
minor 2%
Down’s – 25 (1:1350),
Free HCG
Nuchal translucency
Cameron Korb-Wells & Kai Brown (2009)
35 (1:350), 40 (1:100)
US + bloods = 90%
± 12-14wks
Loss rate 1%
Chorionic villus
(results back faster,
1-2% genetic
mosaicism = false –
If high risk. Miscarriage rate ~ 1:300, thus
recommended when screening test indicates same
(also screen for
NTD via AFP)
20wks should be getting foetal movements, first
palpate uterus at umbilicus.
Morphology scan: Anatomy, placenta, liquor, dating ±
Morphology scan
GDM screening
Challenge Screening: nonfasted 50g over 1hr (norm
OGTT Diagnostic: fasting
75g over 2hr (norm <7.8)
Give anti-D if Rh –ve
(second dose within
72hrs of birth, or at any
antenatal bleeding)
FBC + flim
Rh Ab screen
GBS screening
Wk 37 head engaged
Lower vaginal swab
Cameron Korb-Wells & Kai Brown (2009)
11. Discuss the relevance of nutrition and supplements during pregnancy.
12. Discuss counselling of patients on breast care, posture, diet, smoking, exercise,
sex and drugs during pregnancy.
13. Identify and demonstrate an ability to manage the minor discomforts in pregnancy.
14. Discuss the counselling of a woman about her normal pregnancy.
Normal weight gain is very variable and depends on starting BMI (less gain for higher BMI)
 a normal BMI will gain ~11.5 – 16kg
 not all the weight is lost after birth
Normal pregnancy requires ~ 80,000 calories (↑ daily intake ~100-300 cal.)
 easy recommendation is just to advise patients to maintain a relatively balanced diet,
including plenty or protein, but otherwise eat when and what they want.
 Enquire about diet to screen for absurd fad diets.
 Avoid
o Pate’s, soft cheeses (listeria), avoid vit A and liver, avoid cold salads etc
in displays.
Vitamins / Minerals
 Fe requirement ↑, hard to meet this demand on diet alone, thus recommend
≥27mg of ferrous Fe supplement daily.
 Severe maternal idodine deficiency predisposes to cretinism.
 Folic acid
o 4mg folic acid for month prior to conception and 1 trimester reduces
the risk of neural tube defect.
 Vit B12
o May be lowish in strict vegtarians or those who take excess Vit C
 General principals… humans have been having uneventful pregnancies without
supplements for some time now…..
Fine, although try to avoid malaria-endemic areas
Seatbelt above, under but not over the bump.
If travelling for long periods, ensure calf exercises, good hydrationstockings or
breaks re: DVT risk.
o If risk++ consider pre and post-flight LMWH or aspirin.
 exercise should be maintained at approximately the same level as before pregnancy
 muscle strength and flexibility improve posture and muscle tone and reduce common
discomforts of pregnancy
 aggressive exercise (prolonged jogging and skiing) should be avoided as the
developing fetus can affect balance
Sexual Intercourse
 sexual intercourse may continue throughout pregnancy except in patients at risk for
abortion, preterm labour, or those with placenta previa
 breast stimulation may induce uterine activity and is discouraged in high-risk patients
near term
 labour may follow coitus due to the effect of prostaglandins in the seminal fluid
Incr. risk IUGR, spontaneous abortion, pre-term labour, placental abruption,
perinatal mortality.
Cameron Korb-Wells & Kai Brown (2009)
Foetal alcohol syndrome
o Characteristic facies, growth retardation, intellectual disability.
o No exact dose response
Minor ETOH intake should be OK, but unclear thus recommendation to avoid
Common Complaints
 Backache, esp. in 3 trimester (pressure, muscle + ligament strain)
o Mx – posture
 Bleeding gums due to ↑ blood flow
o Mx – conservative
 Breast enlargement (up to 1-2 cup sizes)
o Mx – supportive bra
 Carpal Tunnel (up to 50% will have mild)
o Mx – fit a wrist splint if severe, most resolve
 Complexion changes
o Brownish/yellowish cholasma
 Mx – nil
 Dizziness (↓ BP)
o Avoid postural changes
 Fatigue (? Hormonal, anaemia)
o Mx – rest, Fe supplement
 Fluid retention (50% incidence, ↑ cortisol, ↓ albumin)
o Mx – rest + leg elevation, supportive stockings
 Hair and nails (↓ shedding during, 50% excessive shedding post-partum)
 Headaches ↑ freq. (↑ oestrogen)
o Mx – conservative, meds last resort
 Morning Sickness (? b-hCG)
o Small meals, cyclizine, steroids
 Nosebleeds
o Saline drops, avoid nasal sprays
 Stress incontinence (pressure)
o Pelvic floor exercises
 Varicose veins
o Discourage prolonged standing and sitting, stockings
Cameron Korb-Wells & Kai Brown (2009)
9. Take a history, examine a pregnant patient attending for a routine visit to the
antenatal clinic and discuss their findings.
3. Perform a vaginal examination on a patient who is less than 14 weeks pregnant and
describe the findings.
7. Palpate the abdomen of a patient after 28 weeks gestation and accurately describe
relevant findings.
1 Antenatal Visit
 Obstetric Hx
 Gyane Hx – LMP, usually length
 Difficulties falling pregnant
 Contraception, other meds
 Other medical illness, concurrent or chronic
 Hx/FHx DVT, DM, thrombophilia, depression/post-natal depression
 Social Hx
 Education
 UA
 Full CVS, resp, BP weight, abdomen
 Vaginal Ex
o Note any masses, blood or D/C
o Note cervical length (normal 3-4cm)
o Note cervical os (closed = nulliparous
o Consider pap smear
Subsequent Visits
 Ask re: symptoms of pregnancy (N/V etc.)
 Ask re: progression of pregnancy
o Growth
o Foetal movements after 20wks (how many per day)
 Ask re: abnormal pains/bleeding
 Ask if any questions
 UA (albumin, glucose) and weight
 BP
 Feel foetal orientation if possible, and later, engagement
 Measure fundal height from fundus to symphisis
 Check foetal HR (120-160) with Doppler.
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to appreciate the pre-conceptual,
antenatal and intrapartum factors, which may adversely affect an embryo or fetus so that they
can initiate the management of related problems.
Obstetric history
o Establish pregnancy if unknown status – delayed menstruation (up to a week, on
a background of previous normal cycles), date of the last period, evidence of
morning sickness, if a home pregnancy test has been used, has it been
confirmed by ultrasound? Other symptoms include breast pain and presence of
foetal movement.
o History of present pregnancy:
 Mother’s age
 Date of last menstrual period
 Weeks gestation
 Expected delivery date
 Planned?
 Symptoms / complications during pregnancy (of importance is:
• Pelvic/abdominal pain
• Vaginal bleeding
• Cramping – suspicion of ectopic or abortions.
• Vaginal discharge (infection)
• Fluid leakage (ruptured membranes) also important
• Some routine problems of pregnancy include
o back pain
o constipation
o dehydration
o oedema
o urinary frequency
• Foetal movement (usually by 16-20 weeks)
• Blurred vision, headache, rapid weight gain
• Any prenatal care received up until now?
• Menstrual history:
o Date of last menstrual period
o Age of menarche
o Regularity
o Abnormal bleeding (amenorrhea, dysmenorrhoea, etc)
o Heavy bleeding / spotting / breakthrough bleeding
o Prior use of the OCP
• Past History
o Obstetrics history of prior pregnancies (parity TPAL) –
 Date
 Outcome
 Mode of delivery
 Length of time in labour
 Birth weight
 Any complications.
o Sexual history – STDs, dyspareunia.
o Other relevant past medical / surgical history.
o Medications – prior to and during pregnancy.
o Allergies
• Family History
o Congenital problems (mother & father’s family)
o Other relevant family history (hypertension, IHD, DM)
• Social History
o Tobacco / EtOH history
o Recreational drugs
o Occupation of both parents
Cameron Korb-Wells & Kai Brown (2009)
Features pertaining to the mother:
o Pre-existing disease
o Increased maternal age (>35)
o Height (<154cm)
o Extreme obesity, social deprivation
o Grand multiparity
o Infection
 +ve serology (TORCHS…)
Features pertaining to previous pregnancies:
o Preterm (<37wks) or small (<2.5kg)
o Deformity, stillbirth, neonatal death
o C/S or hysterectomy
o Retained placenta; abruption
o Pelvic floor damage +/- repair
o Instrumental deliveries
Features of this pregnancy:
o Cardiac or thyroid disease
o Multiple gestation
o Rh –ve with antibodies
o Poor fetal growth or wellbeing
o Diabetes, increased BP, anaemia
o Malpresentations after 34 wks
o Raised alpha-FP
o Placenta previa
o Renal probs
o Clotting abnormalities
Adverse effects of exogenous hormones, drugs, irradiation and infectious conditions
Medications: a number of medications are unsafe to use during pregnancy, risking
fetal malformation/death. Drugs contraindicated by condition include:
• Vitamin A and derivatives
(isotretinoin, etretinate) 
heart/great vessel defects,
craniofacial dysmorphism,
• Tetracycline  discolouration of
• Quinolones  cartilage damage
• Sulfonamides (late) 
• Streptomycin  CN8
• Folic acid antagonists 
craniofacial abnormalities
• Thalidomide  limb reduction
and ear/kidney/heart
Cameron Korb-Wells & Kai Brown (2009)
• Benzoyl peroxide
• Penicillins/ cephalosporins/
• Alkylating agents used 2 /3
• Pyroxidine/ doxylamine/
metoclopramide/ ondansetron/
(NB risks trauma,
• Lithium  congenital heart
disease and Ebstein’s anomaly
• SSRIs  may cause persistent
pulmonary hypertension, poor
feeding +/- jitteriness
• Aspirin  avoid late pregnancy
as risk of bleeding, close PDA;
• Ergotamines  abortifacient
potential and risk fetal
• ACE-I/ARBs  fetal renal
damage and oligohydramnios
• Beta-blockers: propanolol
• NSAIDs  avoid late pregnancy
for >48 hours, if used for
prolonged period may
prematurely close DA
• Phenytoin  facial dysmorphism,
microcephaly, mental retardation,
hand hypoplasia, NTDs
• Valproic acid  craniofacial
defects and NTDs
• Carbamazepine  craniofacial
defects, mental retardation, NTDs
• Phenobarbital  cleft palate,
cardiac defects
• Trimethadione  strong
teratogenic potential with mental
retardation, speech difficulty,
abnormal facies
• Warfarin  fetal nasal hypoplasia
and chondrodysplasia
Consider risks v benefits of
Consider risks v benefits of
• Paracetamol/ codeine/ caffeine
• Labetalol/ hydralazine/ nifedipine/
methyldopa/ clonidine
• Panadol/ morphine/
hydrocodone/ propoxyphene
SAFE though should not be used
Use agent works best to
control maternal seizures
Monotherapy at lowest dose
Folate supplementation 3
months prior to conception
Sleep deprivation in last month
of pregnancy may contribute to
• Heparin, LMWH
Must use warfarin in cases of
highly thrombogenic artificial
cardiac valves (risk/benefit
Radiation: diagnostic and nuclear medicine studies pose no risk of fetal
teratogenicity if overall exposure during pregnancy is <5000 mrads (0.05 Gy)
o Abdo XR (1 view)
100 mrad
o CXR (2 views)
0.02-0.07 mrad
o CT head/chest
<1000 mrad
o CT abdo/lumbar
3500 mrad
CONSIDER infections that increase or whose complications increase in
pregnancy, infections specific to pregnancy and infections that can affect the
o Increased complications in pregnancy: UTI, bacterial vaginosis, surgical
wound, GBS
o More common in pregnancy: pyelonephritis, endomyometritis, mastitis,
toxic shock syndrome
o Specific to pregnancy: chorioamnionitis, septic pelvic thrombophlebitis,
episiotomy/perineal lacerations
Cameron Korb-Wells & Kai Brown (2009)
Affecting fetus: neonatal sepsis (GBS, E coli), HSV, VZV, PV B19, CMV,
rubella, HIV, HBV/HCV, gonorrhoea, chlamydia, syphilis, toxo)  remember
 T
 O
Other (Parvo B19)
 R
 C
 H
 S
Background: incidence increases during pregnancy. Asymptomatic
bacteruria (>100,000 colonies on culture) in ~5% all pregnancies  higher
rates of cystititis and pyelonephritis in pregnant women (25-40% progression)
 Specific RISKS: preterm birth, low birth-weight infants
 Pathogenesis: multifactorial, progesterone-mediated SM relaxation
(decreases bladder done and causes ureteral dilation), mechanical
compression from enlarged uterus (ureteral obstruction  stasis)
o Dx: clinical signs and symptoms of dysuria, frequency and urgency with
positive culture. U/A often used as proxy until cultures returned (leukocyte
esterase, nitrates or haematuria)
o Rx: E coli >70%, remainder Klebsiella, Enterococcus, Proteus, coagnegative Staph and GBS
 Empiric Rx (E coli predominance): amoxicillin, TMP/SMX or
cephalexin, nitrofurantoin
 Duration: 3-7 day course, though many prefer 7 days for pregnancy
(adjusting on culture and sensitivities)
o F/U: as may persist, obtain test of cure culture 1-2 weeks postcommencement of therapy.
o Background: up to 1-2% pregnancies, with potential complications of septic
shock and ARDS
o Rx: aggressive with hospitalisation, IV hydration, IV ABx  cephalosporins
(cefazolin/cefotetan, ceftriaxone) or amp + gentamicin
 Duration: until patient afebrile and asymptomatic for 24-48 hours
 Transition oral ABx regimen
 Duration: total 14 days treatment
o Prophylaxis: pregnant patients with one episode of pyelonephritis or two or
more episodes of asymptomatic bacteuruia and/or cystitis generally placed
on ABx prophylaxis for duration of pregnancy
Bacterial vaginosis
o Background: BV increases risk of preterm premature rupture of membranes,
preterm delivery and puerperial infections
o Clin: malodorous discharge/ vaginal irritation, though may be asymptomatic
o Dx: 3 of 4 of  (1) clinical findings of thin, white, homogenous discharge on
vaginal walls OR (2) amine odor with addition of 10% KOH (“whiff” test) OR
(3) pH>4.5 OR (4) clue cells on microscopic examination
 Gram stain (gold standard): Gardnerella vaginosis, Bacteroides,
Mycoplasma hominis
o Rx: metronidazole PO preferred (clindamycin PO alternate, clindamycin PV
C/I due to adverse fetal effects)
o F/U: test of cure 1/12 after completion
o Background: contributor to UTI/ chorioamnionitis/ endomyometritis during
pregnancy, as well as neonatal sepsis  2-3 per 1,000 LB
 Mortality rate GBS sepsis 5-50% (depending on gestation at delivery)
o Screening: to protect infants from GBS, with rectovaginal culture for GBS
colonisation between 35-37 weeks
o Dx: high vaginal smear and MCS screen 35-37 weeks
o Rx: if positive, IV penicillin G intrapartum
 Also for <37 weeks or unknown status with ROM >18 hours
Cameron Korb-Wells & Kai Brown (2009)
 Penicillin allergy: cefazolin OR clindamycin for severe allergy
o Background: infection of membranes/amniotic fluid, associated with preterm
and prolonged ROM, most common precursor of neonatal sepsis with high
rate fetal mortality. Also maternal sequelae  endomyometritis/septic shock
o Clin: maternal fever, elevated WCC, uterine tenderness, fetal tachycardia
 Exclude conditions with similar clinical picture (other loci of maternal
infection, fever with IOL using PGs/ epidurals, corticosteroids)
o Dx: in patients at term, if clinical signs exist without any other aetiology, Dx
should be presumed and treatment started. If pre-term, definitive testing:
 Amniocentesis (gold standard): culture amniotic fluid, test glucose,
WCC, protein and Gram stain (sensitivity 40-70%)
 IL-6 in amniotic fluid: produced by infected fetus’ immune
response, raising prior to other tests though only experimental
o Rx: IV ABx, broad spectrum, second/ third generation cephalosporin OR
amp+gentamicin (vaginal/ rectal flora)
 Hasten delivery with induction/augmentation or CS if non-reassuring
o Background: DNA virus, subtypes HSV-1&2  HSV-2 predominantly
causes genital herpes. Can produce severe infection in neonate, with risk
50% in primary maternal infection and 1-5% in recurrent. HSV encephalitis.
o Clin: patients with history of herpes should have thorough perineal exam for
lesions when presenting in labor for risk of vertical transmission
 Consider primary versus recurrent infections: primary infections
in pregnancy have much higher fetal attack rate (transplacental
during viraemic illness)  if transmitted 3 trimester, particularly
dangerous as lack of maternal antibodies transmitted to fetus
 Neonate: may progress to viral sepsis, pneumonia, herpes
o Dx:
 Mother: differentiate primary v secondary infection with Ig titers 
IgM and type-specific IgG (latter present if prior infection). Does not
change Rx/ outcome: does affect prognosis/ counselling
 Neonate: viral cultures of herpetic lesions, oropharynx or eyes
o Screening: large proportion of HSV-infected women unaware, proposed
universal screening though expensive with ? little benefit
o Rx
 During pregnancy: HSV genital outbreak during pregnancy 
acyclovir prophylaxis from 36/40 to delivery to prevent recurrent
 At delivery: if lesions are present, C/S is recommended mode of
delivery  prevent vertical transmission
 Neonate: IV acyclovir as soon as infection suspected
o Background: DNA herpes virus, >90% adults immune (childhood disease),
more serious in adults with higher rate varicella pneumonia. Vertical
transmission transplacentally  congenital malformations of congenital
varicella syndrome in 0.5-2% cases with infection 8-20/40
o Clin: exposure 8-20/40  congenital varicella syndrome, late-term exposure
 benign/ chickenpox OR fulminant and death
o Dx: VZV titers during pregnancy for patients unsure about exposure history
o Rx:
 Preconceptually: screen for VZV titers and if negative immunise
prior to conception
 VZIG: to patients without Hx chickenpox with exposure in pregnancy,
within 96 hours of exposure AND to infants of mothers developing
varicella disease within 5 days before delivery or 2 days after
Parvovirus B19
Cameron Korb-Wells & Kai Brown (2009)
Background: erythema infectiosum (fifth disease) with red macular rash on
face (slap-cheek) resolving spontaneously. Risk maternofetal transmission in
nd rd
pregnancy  fetal infection and death. 1 trimester  miscarriage. 2 /3
trimester  fetal hydrops attacking fetal erythrocytes causing haemolytic
anaemia, hydrops and death
Dx: if exposure suspected, check parvovirus IgM and IgG
Rx: if acute infection (+IgM, +/- IgG) >20 weeks, serial U/S 8-10 weeks after
maternal infection (? Doppler of fetal MCA to detect anaemia), fetal
transfusion where evidence of hydrops
Background: usually subclinical in mother, rarely hepatitis/ mononucleosislike syndrome in utero infections ~1% all newborns, with ~10% of those
symptomatic at birth
o Clin neonate: hepatomegaly, splenomegaly, thrombocytopaenia, jaundice,
cerebral calcification, chorioretinitis, interstitial pneumonitis  mortality rate
~30%, +/- mental retardation, sensorineural hearing loss,
neuromuscular disorders. Of asymptomatic, 15% late disabilities and 85%
no sequelae
o Rx: no Rx or prophylaxis. Are studies reporting IV hyperimmune globulin and
antivirals though evidence lacking. Vaccine being investigated.
o Background: adults  maculopapular rash/ arthritis/ arthralgias/ diffuse
lymphadenopathy 2-4 days. Fetal transmission  congenital rubella
syndrome, with highest risk 1 trimester.
o Clin congenital rubella syndrome: deafness, cardiac abnormalities,
cataracts, mental retardation, any organ system if infected during
organogenesis (delayed onset diabetes, thyroid disease, deafness, ocular
disease, growth hormone deficiency)
o Screening: check rubella titer during 1 trimester
o Dx: serology  IgM titers (does not cross placenta so if present indicates
infection), IgG supportive
o Rx: nil once acquired, though immunisation has decreased incidence. Unimmunised women should avoid anyone with possible infection.
 MMR live vaccine so avoid until postpartum, and avoid pregnancy for
1/12 following vaccine
o Background: with no Rx, ~25% infants to HIV-infected mothers become
infected. Transmission increased with higher viral burden/advanced disease
in mother, ROM and invasive procedures increasing neonatal exposure to
maternal blood. Transmission either in-utero (1/3) in late pregnancy or during
delivery (2/3). Also 2-year infection rate from breast milk ~15%
o Screening: first prenatal visit and again in 3 trimester if specified risk factors
o Rx: HAART with triple regimen started 2 trimester reduces risk of
transmission <1-2%
 Consider C/S if viral load >1,000/mL and without long-standing
onset of labor or ROM. C/S lowers transmission rates ~2/3 cf vaginal
delivery in those with no therapy or high viral load.
 ? Breastfeeding
o Background: PID early pregnancy, preterm delivery, PPROM, puerperial
infections. Neonatal transmission via birth canal, affecting eye/ oropharynx/
external ear/ anorectal mucosa  may disseminate  arthritis/ meningitis
o Screening: first prenatal visit and again 3 trimerster for high-risk
o Dx: PCR or culture
o Rx: ceftriaxone IM, cefixime PO, spectinomycin IM (where cephalosporin’s
not tolerated)
 Azithromycin/ amoxicillin for presumed Chlamydia as well
Cameron Korb-Wells & Kai Brown (2009)
Background: transmission via birth canal, in infected women with vaginal
deliveries  neonatal sequelae of conjunctivitis (40%), chlamydial
pneumonia (10%)
Screening: asymptomatic infection common therefore screen all at first visit
and again 3 trimester if high-risk
Rx: azithromycin, amoxicillin or erythromycin (tetracycline/ doxycycline C/I in
Background: transmission sexually/ blood-borne/ transplacentally. Clinically
mild hepatic dysfunction to fulminant liver failure and death.
o Screen: prenatally all patients for HbSAg (if +, likely chronic disease and at
risk of transmission)
o Rx:
 Mothers: if exposed during pregnancy, PEP with HBV IVIG and
complete HBV vaccine series recommended
 Neonates: HBV IVIG at birth (within 12 hours) and HBV vaccination
at birth, 1 month and 6 months (routine)
o Background: sexual transmission or transplacentally to fetus, >70% of
infants born to mothers with untreated syphilis will become infected, cf 1-25
of those receiving adequate Rx. Exposure  late abortion, intrauterine fetal
demise or congenitally infected infant
o Clin congenital syphilis: maculopapular rash, snuffles, hepatomegaly,
splenomegaly, haemolysis, lymphadenopathy, jaundice
 Late congenital syphilis (if untreated): CN8 deafness, saber shins,
mulberry molar, Hutchinson’s teeth, saddle nose
o Dx: IgM antitreponemal antibodies (do not cross placenta)
o Rx: penicillin
o Background: common protozoa, usually subclinical infection (occasionally
fevers, malaise, lymphadenopathy, rash), though pregnant women may
transmit transplacentally  more common in 3 trimester though more
serious in 1 trimester.
o Clin congenital toxoplasmosis infection: fevers, seizures, chorioretinitis,
hydro- or microcephaly, hepatosplenomegaly and jaundice
o Prophylaxis: avoid cat litter boxes and significant gardening without glove
and mask protection
o Dx:
 Fetal: amiocentesis and PCR for T gondi 4 weeks after maternal
 Neonate: toxoplasmosis IgM (though absence does not rule out),
use reference laboratory
o Rx:
 Mother: spiramycin, though does not cross placenta, consider
termination if contracted in first two trimesters
 Fetal: pyrimethamine + sulfadiazine, with folic acid
Application, risks and information derived from use of CVS, amniocentesis, XR and
• U/S-guided transabdominal extraction of amniotic fluid
• Indications
o Genetic abnormalities, e.g. trisomies (15-16/40)
o Fetal lung maturity (third trimester) - L/S ratio (lecithin:sphingomyelin): if >
2:1, fetal lungs are mature enough that respiratory distress syndrome (RDS)
is less likely to occur
o Bilirubin concentration in Rh-isoimmunized pregnancies
• Advantages
o Screens oNTD (acetylcholinesterase and amniotic AFP)
Cameron Korb-Wells & Kai Brown (2009)
o More accurate genetic testing
o 0.5% risk of spontaneous abortion
o Results take 10-14 days; FISH available in 72 hours
Risk/benefit: >35 years, risk of chromosomal anomaly (1/180) greater than
increased risk of miscarriage from the procedure, so offered routinely
Needle through abdomen or catheter through cervix at 10-12 weeks for CVS
o Chorion of fetal origin, so cells obtained examined as amniocentesis
o Enables pregnancy to be terminated earlier
o More rapid karyotyping, DNA tests, chromosome status,
o Biochemical assay (results in 48 hours; do not have to wait for culture)
o Increasing availability of probes to allow diagnosis of genetic abnormalities
(i.e. FISH)
o High sensitivity and specificity
o 1-2% risk of spontaneous abortion
o Does not screen for neural tube defects (NTD)
o Risk of limb injury
o 1-2% incidence of genetic mosaicism ––> false negative results
• Dating: for unknown or uncertain LMP, most accurate in first trimester (~8 weeks).
Alters EDC if dates uncertain and >1 week discrepancy
• Fetal malformation detection: routine morphology scan 18-20 weeks
• Routine testing: placental location, amniotic fluid volume, gestational age, obvious
malformations, +/- sex determination (indicated for X-linked disorders)
• High risk pregnancies in 3 trimester
o Fetal growth
o Fetal Doppler: assess flow in umbilical cord  decrease/ absence/ reversal
of diastolic flow in umbilical artery more concerning for placental insufficiency
o Biophysical profiles (BPP): score 0-2 for each of  amniotic fluid volume,
fetal tone, fetal activity, fetal breathing movements, nonstress test (FHR)
 BPP ≥8-10 reassuring
• Risk estimate of whether the fetus may be affected with Down Syndrome, trisomy
18, or an open neural tube defect (oNTD)
o 80% of Down’s babies born to women under 35 years, so valuable screening
o Other chromosomal abnormalities not detected; therefore still offer
amniocentesis/chorionic villous sampling (CVS) to high risk women
• Results highly dependent on gestational age, so accurate dating important for
accurate diagnosis  positive MSS should be followed up with U/S and/or
• Three markers: maternal serum alpha-feto protein (MSAFP), ßhCG, unconjugated
estrogen (uE3)
• Results
o Trisomy 21: low MSAFP, high ßhCG, low uE3
o Trisomy 18: low MSAFP, low ßhCG, low uE3
• Stats
o Sensitivity for Down Syndrome detection: 60%
o Sensitivity for oNTD: 80-90%
o MSS has a 9.5% false positive rate if maternal age >35; lower false positive
rate for oNTD and T18
Cameron Korb-Wells & Kai Brown (2009)
Signs during pregnancy indicating fetal malformation
• Signs:
o Amniotic fluid volume
o Decreased fetal movements
o PV bleeding/ discharge
• Ectopic pregnancy: (1%, most tubal)
o Unilateral pain, bleeding
o Dx: Ultrasound
o Rx:
 Ruptured: Remove, stabilize
 Unruptured: Methotrexate
• Spontaneous abortion:
o 1 trimester:
 Rule out ectopic, complete with D+E (or expectant Mx) up to 3/40:
incomplete, missed, inevitable, Rho-GAM to Rh-ve mums.
o 2 trimester:
 secondary to uterine/cervical abnormalities, trauma, systemic disease or
 Rx: D+E, prostaglandins or oxytocic agents to assist completion if
• Incompetent cervix (painless dilation):
o Risk factors:
 Surgery, cone biopsy, lacerations in previous vaginal delivery, uterine
anomalies, DES exposure
o Can cause: infection, PPROM, Preterm labour
o Previable fetus: expectant Mx, elctive termination, or immediate cerclage
o Previous Hx: elective cerclage offered at 12-14 weeks
• Antepartum haemorrhage
• Fetal vessel rupture
• Pre term labor:
o Rx: tocolytics, (Mg, Ca blockers, NSAIDS), Betamethasone
o Continue as long as possible up to ?36 weeks with close monitoring of fetus.
o Rx: corticosteroids and ampicillin (+- erythromycin); Delivery if signs of infection
Formation, constitution and significance of amniotic fluid
• Formation
o Late gestation much of the amniotic fluid consists of fetal urine
o Continually swallowed and "inhaled" and replaced through being "exhaled",
as well as being urinated. Essential that amniotic fluid breathed into lungs for
normal lung development. Swallowed amniotic fluid contributes to the
formation of meconium.
• Constitution
o Proteins, carbohydrates, lipids and phospholipids, urea and electrolytes
 Support fetal growth
• Oligohydramnios: AFI ≤5cm on U/S
o Causes: fetal urinary tract abnormoalities (renal agenesis, polycystic
kidneys, urinary obstruction), chronic uteroplacental insufficiency, rupture of
o Dx: U/S for abnormalities, rule out ROM with Ferning test/nitrazine pH paper
o Rx: delivery
o Complications: cord compression  fetal hypoxia, musculoskeletal
abnormalities (facial distortion, clubfoot), pulmonary hypoplasia, IUGR
• Polyhydramnios: AFI ≥25cm on U/S
o Causes: normal pregnancy, uncontrolled maternal DM, multiple gestation,
pulmonary abnormalities, fetal anomalies (duodenal artresia, TOF)
o Dx: U/S for fetal abnormalities, glucose testing for DM
o Rx: depends on cause, therapeutic amniocentesis
Cameron Korb-Wells & Kai Brown (2009)
Complications: preterm labour, placental abruption, fetal malpresentation,
cord prolapse
Induction of labour, vaginal delivery or CS adverse effects on the fetus
• Induction of labor:
o Indications: post-term pregnancy, preeclampsia, PPROM, nonreassuring
fetal testing, IUGR
o Preparation: form a plan for induction, success is correlated with favourable
cervical status (Bishop score >5  failure ~50%)
 PGE2 gel/pessary or misoprostol to ripen/dilate the cervix (C/I
maternal  asthma, glaucoma; C/I neonatal  >1 prior C/S,
nonreassuring FHR), risk uterine hyperstimulation
 Mechanical means: 30/60 cc Foley bulb inside cervix, placed on
gentle traction
o Induction: formally begins pharmacologically with oxytocin IVI, or amniotomy
(though examine to ensure no cord prolapse)
• Augmentation of labor: oxytocin and amniotomy
• Vaginal delivery:
o Assisting
 PPE: goggles/ sterile gown/ sterile gloves
 Equipment: two clamps, scissors, suction
 Smooth, controlled delivery  less perineal trauma
• One hand controls ascent of fetal head through introitus
• Other hand may minimise torsion on perineum to prevent
 If meconium in amniotic fluid, suction applied to nares and mouth for
vigorous suctioning before delivery of shoulders
 Check for nuchal cord, and reduce over infant’s head. If too tight, two
• If extremely confident that delivery imminent, may clamp and
cut cord
• If shoulder dystocia suspected, attempt delivery with nuchal
cord intact
 Anterior shoulder delivered by downward pressure on head
 Posterior shoulder delivered by upward pressure
 Gentle traction to deliver torso and rest of infant
 Clamp cord and cut, passing to mother
• Caesarian
o Indications
 Maternal/fetal:
• Cephalopelvic disproportion
• Failed induction of labor
 Maternal
• Severe pre-eclampsia / eclampsia
• Cervical cancer
• ?Prior uterine surgery
• Obstruction (fibroids, tumour)
 Fetal:
• Non-reassuring testing
• Scalp pH < 7.2
• Cord prolapse
• Malpresentation (breech, transverse lie, brow)
• Multiple gestation (non vertex 1 twin, >2 babies)
• Fetal anomalies (hydrocephalus, osteogenesis imperfecta)
 Placental:
• Placenta previa
• Abruptio placentae
o VBAC: may be attempted where proper setting exists, including obstetrician,
anaesthetist and surgical team with informed patient consent
 Risk: rupture of prior uterine scar, ~0.5-1.0%
Cameron Korb-Wells & Kai Brown (2009)
Higher rates with induction, thus require adequate
counselling and consent for induced VBAC trial
C/I: vertical incision through upper segment or multiple C/S deliveries
Uterine rupture: associated with previous uterine scar (in 40% of
cases), hyperstimulation with oxytocin, grand multiparity and
previous intrauterine manipulation
• Management: immediate delivery for fetal survival, maternal
stabilization (may require hysterectomy)
• Complications: maternal mortality 1-10%, maternal
hemorrhage and shock, DIC, amniotic fluid embolus,
hysterectomy, fetal distress ––> 50% mortality
Perinatal mortality and major contributing factors
• Abortion: loss of intrauterine pregnancy prior to viability of fetus
o < 20 weeks and/or < 500 g fetal weight
o Includes induced (therapeutic) and spontaneous (miscarriage)
• Stillbirth: loss of intrauterine pregnancy after 20 weeks and/or > 500 g fetal weight
• Stillbirth Rate: annual number of stillbirths per 1,000 total births
• Perinatal Mortality Rate: the annual number of stillbirths and early neonatal deaths
(in the first seven days of life) per 1,000 total births
o Prematurity
o Congenital anomalies
• Neonatal Mortality Rate: annual number of deaths of liveborn infants within 28 days
per 1,000 live births
• Infant Mortality Rate : the annual number of deaths of liveborn infants in the first
year of life per 1,000 live births (includes neonatal mortality)
• Maternal Mortality Rate: annual number of deaths of women while pregnant or
within 90 days of pregnancy per 100,000 live births
o Direct: from obstetrical causes such as ectopic, pregnancy induced
hypertension (PIH), post partum hemorrhage (PPH), infection, pulmonary
embolus (PE)
o Indirect: from pre-existing illness or by accident
• Birth Rate: the annual number of live births per 1,000 population
• Fertility Rate: the annual number of live births per 1,000 women aged 15-44 years
Cameron Korb-Wells & Kai Brown (2009)
1. Discuss the significance of abnormalities of uterine size and shape, or lie and
presentation of the foetus by clinical examination of the abdomen of a pregnant
Fundal height should = dates ± a few weeks
o Deviation from this may indicate IUGR or oligohydramnios
Foetal lie is either transverse or longitudinal (99%)
Presenting part is either cephalic or breech
Cephalic presentation is either occiput, sinciput, brow or face presentation
The station is te extent to which the presenting past has descended into the
pelvis by 5ths
2. Discuss the principles of the immediate management of the patient with
antepartum haemorrhage.
5. Discuss the cause and prophylaxis of rhesus iso-immunisation in pregnancy and the
principles of management.
 Serious causes – abruption, placenta praevia, vasa praevia
 Abortion (threatened, inevitable, incomplete, complete)
o < 5% of threatened abortions go on to abort
 Abnormal pregnancy (ectopic, molar)
 Trauma (post-coital)
 Genital lesion (e.g. cervical polyp, neoplasms, varicosities, )
Placenta Praevia
 <1% maternal mortality
 4-8% recurrence risk
 Presents with PAINLESS bright red blood
 Uterus soft and non-tender
 After, limit physical activity, no sex
 Presents with sudden PAINFUL bright red blood, uterine contractions
 Part of placenta comes apart from uterus, cause usually unknown
o May occur secondary to pre-eclampsia.
o Recurrence rate 10%
 Placental insufficiency may cause hypoxia or death.
 Compression of uterine muscles may prevent adequate contraction so ↑ risk PPH
 Posterior abruptions may cause backache.
 Thromboplastin release may cause DIC.
Management of APH
“Any antepartum bleed is likely to be a very distressing time for the mother. Whilst most
bleeds are inconsequential, any APH is associated with ↑ risk of perinatal mortality and may
indicate spontaneous abortion. APH can also lead to severe life-threatening haemorrhage.
My steps in management would be…”
1. Assess ABC and resus
Cameron Korb-Wells & Kai Brown (2009)
2. Take bloods, send for blood
3. Mild
a) Establish Dx (US ± speculum)
4. Severe
a) Catheterise to measure UO if severe
b) Call expert help
c) Deliver and beware PPH
1. Assess ABC and resus
a. Check airway
b. Give 15L/min O2, measure SaO2
c. BP, HR, cap refil - 2x 18g, take off bloods, legs up, IV fluids. Maintain sBP >
d. GCS
e. Trauma
f. Foetal monitoring (CTG)
2. Take bloods, send for blood
FBC, UEC, LFT, Coags, Group and crossmatch
Send for compatible or O-ve blood (6U)
5. Mild
Regular Obs, chart blood loss, replace with blood
Establish exact diagnosis
Placenta previa – keep until 38 wks then LSCS
If is a bleed from small abruption that settles and no foetal compromise – observe
then send home (after anti-D if indicated)
 Treat as high risk, arrange F/U
6. Severe
Mainatian UO > 30mL/hr
Get anaesthetist and expert help
If bleeding is severe – consider steroids for foetal lungs, LSCS (BEWARE PPH)
 antibodies produced against a specific RBC antigen as a result of antigenic stimulation
with RBC of another individual
 most common is anti-Rh Ab produced by a sensitized Rh-negative mother (more than
90% of cases of Rh isoimmunization are due to D antigens)
 other antibodies can lead to fetal red blood cell hemolysis
o much less common and no prophylaxis is available
 overall risk of isoimmunization of an Rh-negative mother with a Rh-positive ABOcompatible infant is 16% (2% of reactions will occur antepartum, 7% within 6 months of
delivery, and the remainder 7% in the second pregnancy)
 maternal-fetal circulation normally separated by placental barrier
 upon first exposure, initially IgM and then IgG antibodies are produced
 sensitization routes
Cameron Korb-Wells & Kai Brown (2009)
incompatible blood transfusion
previous fetal-maternal transplacental hemorrhage
invasive procedure while pregnant
therapeutic abortion, D&C, amniocentesis
during labour and delivery
 routine screening at first visit for blood group, Rh status, antibodies
 Ab titres < 1:16 considered benign
 Ab titres > 1:16 necessitates amniocentesis (correlation exists between amount of biliary
pigment in amniotic fluid and severity of fetal anemia) from 27 weeks onwards
 Liley curve is used to determine bilirubin level and appropriate management
 Kleihauer-Betke test can be used to determine extent of fetomaternal hemorrhage
o fetal red blood cells are identified on a slide treated with citrate phosphate
o adult hemoglobin is more readily eluted through cell membrane in presence
of acid
 detailed U/S for fetal hydrops
 Rhogam binds to Rh Ag of fetus and prevents it from contacting maternal immune system
 Rhogam (300 µg) must be given to all Rh negative women
o at 28 weeks
o within 72 hours of the birth of an Rh positive fetus
o with a positive Kleihauer-Betke test
o with any invasive procedure in pregnancy
o in ectopic pregnancy
o with miscarriage, therapeutic abortion (50 ug)
o with an antepartum hemorrhage
 if Rh neg and Ab screen positive, follow mother with serial monthly Ab titres throughout
pregnancy +/– serial amniocentesis as needed (Rhogam of no benefit)
Management of Rh iso-immunisation
 falling biliary pigment warrants no intervention (usually indicative of fetus which is
unaffected or mildly affected)
 rising or stable biliary pigment on serial amniocentesis must be compared to a standard
table which is divided into 3 zones based on severity of hemolysis (Liley Curve)
 cordocentesis for fetal Hb; should be used cautiously, not first line
 intrauterine transfusion of O-negative packed red blood cells may be required for severely
affected fetus or early delivery of the fetus for exchange transfusion
 anti-Rh IgG can cross the placenta and cause fetal RBC hemolysis resulting in fetal
anemia, CHF, edema, and ascites
 severe cases can lead to fetal hydrops (total body edema), or
 erythroblastosis fetalis
Cameron Korb-Wells & Kai Brown (2009)
3. Discuss the diagnosis, investigation and management of suspected intrauterine fetal
growth retardation.
4. Understand the principles of assessing fetal well being and your clinical application
in the diagnosis and management of a compromised fetus.
IUGR (<10 percentile for gestational age)
 Maternal causes
o Multiple pregnancy
o Malformation
o TORCH Infection
o Smoking
o Diabetes
o Anaemia
o Pre-eclampsia
o Heart or renal disease
o Asthma
 Asymmetric growth restriction due to placental insufficiency leaves the head
relatively spared.
 In adult life, ↑ risk of
o Autoimmune thyroid disease
 symmetric/Type I (20%)
o occurs early in pregnancy
o inadequate growth of head and body although head:abdomen ratio may be
o usually associated with congenital anomalies or TORCH
 asymmetric/Type II (80%)
o occurs late in pregnancy
o brain is spared, therefore the head:abdomen ratio is increased
o usually associated with placental insufficiency
o more favorable prognosis than Type I
 Fundal height measurements at every antepartum visit
o more thorough assessment if mother is in high risk category or if SFH lags >
2 cm behind GA
 U/S exam
o assessment of BPD, head and abdomen circumference, head:body ratio,
femur length and fetal weight
o doppler analysis of umbilical cord blood flow
Cardiotocography (CTG)
 Normal HR 110-160bpm, variability of >5bpm (response to vagal tone, stimuli etc – loss
of variability i.e. smoother line, may reflect sleep or hypoxia or drug effects), ≥2
accelerations of an amplitude ≥15bpm over a 20min period.
o Baseline Tachy – maternal fever, choriamnionitis, B-ergic drugs,
acute/subacute hypoxia. Rate >200 = arrhythmia
o Baseline brady – hypoxia, heart block or cord compression (if spasmodic).
o Early decelerations – with uterine contractions reflect ↑ vagal tone as ICP ↑
o Late decelerations – when trough of decel occurs well after uterine peak
contraction, this reflects foetal hypoxia.
Cameron Korb-Wells & Kai Brown (2009)
Management of a poor CTG trace
o Lay mother on left side and give O2
o Stop oxytocin
o If uterine hypercontractility give tocolysis (terbutaline)
o Take foetal blood sample (scalp) or consider delivery if no CTG improvement.
most important is to get accurate gestational age
Prevention via modifiable risk factors
Bed rest in left lateral decubitus position.
Serial US
Those with abnormal Doppler flows may benefit from low dose aspirin
Delivery when risk of intrauterine life > extrauterine life
o Get expert help
o LCSC as IUGR tolerates VD poorly
o Transfer to specialised nursery post-delivery
Cameron Korb-Wells & Kai Brown (2009)
6. Describe the causes of preterm labour in a patient and discuss her management.
7. Discuss the causes of preterm rupture of the membrane, its differential diagnosis
and management.
Definition: those born <37 weeks
6% singletons, 46% of twins, leading cause of perinatal morbidity and mortality.
 40% unknown
o Bacterial vaginosis ma be risk factor/marker.
o Fish oil may ↓ risk.
 10% multiple pregnancy
 25% APH, cervical incompetence, amnionitis, DM, polyhydramnios, UTI
Risk factors
 Prior Hx (recurrence risk 17-40%)
 Hx of abortions or stillbirths
 Maternal age <18yrs or >40yrs
 Infection (GU or chorioamnionitis)
 Medical illness (HTN, DM, other)
 Mechanical (fibroids, incompetent cervix)
 Previous surgery on uterus (LSCS or cone section)
 Previous surgery on abdo
 Social (low SES, smoking, nutrition, drugs/ETOH, stress/anxiety)
 Maternal-foetal
o PROM (80% will go into labor), polyhydramnios
o Placenta praevia or abruption
 Foetal
o Multiple gestation
o Congenital abnormalities
 Regular contractions (2 in 10min)
 Cervix >2cm dilated or 80% effaced or documented change
Management of Preterm Labour
50% of contractions stop spontaneously
Disability rate 25% <28wks; 12.5% 28-20wks.
o 10% < 28wks who survive will never walk or communicate intelligibly with
o Only 4% of babies <24wks survive, 50% have severe disability.
Are these Braxton-Hicks?
Tocolysis is unlikely to succeed if ROM or cervix >4cm.
Tocolysis has not been shown to be of any benefit
o Except nifedipine when wanting to allow steroids to work or for transfer.
o CI in infection or foetal death/abnormality, pre-eclampsia or APH
24-34 wks - Steroids (2x Betamethasone 12mg IM, 12hrs apart)
o Monitor BSL
o Lowers RDS by 40-50%
o Also helps close ductus and periventricular leukomalacia
Management of PROM
1. Admit and initial Ix
Cameron Korb-Wells & Kai Brown (2009)
Do regular Obs and CTG
Do MSU, UA, high vaginal swab with sterile speculum
If liquor not obvious – test with nitrazine sticks (pH stick)
2. Assess for causes/associations
Do screening for TORCH
Do U/S for bleeding
3. Go to delivery or delay with ABx
If labour progresses, don’t try and stop it
Prophylactic ABx may be considered, esp if pre-labour ~24hrs
o ↓ rates of intraventricular haemorrhage, periventricuclar leukomalacia
Cameron Korb-Wells & Kai Brown (2009)
8. Define hypertension and abnormal weight gain in a pregnant patient.
9. Identify medical conditions in pregnancy requiring specialist care - hypertension,
renal disease (including urinary tract infection), cardiac disease, diabetes, anaemia,
SLE and Idiopathic thrombocytopaenia (ITP).
10. Understand diagnostic criteria for pregnancy induced hypertension and discuss
the principles of its management.
11. Understand the significance of bacteriuria in pregnancy and discuss its
12. Understand the diagnosis of gestational diabetes and discuss the principles of
management of diabetes during pregnancy.
13. Identify medical and psychiatric conditions in pregnant patients necessitating
specialist care.
May be transient, chronic HTN, chronic with superimposed pre-eclampsia or preeclampsia (6% incidence)
Pre-existing chronic HTN
o Drugs may have to be changed (some ↓ foetal growth)
o 5x risk pre-eclampsia (suspect if BP ↑ 30/15, proteinuria, hyperuricemia or
o Pregnancy induced HTN with proteinuria ± non-dependant oedema
 BP >140/90 and proteinuria > 1+ or >0.3g/24hrs
• Proteinuria a late sign (of renal involvement), may measure
urate levels to detect earlier.
 Non-dependant oedema is usually generalised and assoc. with
excessive (>2kg/wk) weight gain.
 Usually develops after 20wks and resolves within 10 days of delivery.
 Severe cases (esp. >160/110) may present with;
• Resp - APO, cyanois
• Cardiac - Cardiac failure
• Renal - ↑ creat., oliguria
• Hepatic - ↑LFTs, RUQ or epigastric pain (subcapsular
haemorrhage), ascites, ↑bilirubin, HELLP
o HELLP Sx – haemolysis, elevated LFTs, Low Plt
• Neuro – visual disturbance, ↑ reflexes, clonus, H/A,
convulsions (“eclampsia”)
• GIT – severe N/V
• Haematological – thrombocytopenia, microangiopathic
haemolysis, DIC.
• Foetal - IUGR
o May present with ‘flu-like illness, headache, chest or abdo pain…N/V, ↑HR ±
visual disturbance, hyperreflexia and irritability.”
 Death occurs from stroke, liver, heart or renal failure.
o Due to failure of trophoblast to invade spiral arteries and protect placental
blood flow  HTN partly compensates for this.
o Risk Factors
 Primip (80-90%)
 Past or FHx of pre-eclampsia
 <155cm tall, ↑ BMI
 Age <20 or >35
 Past migraine
Cameron Korb-Wells & Kai Brown (2009)
Pre-existing HTN, DM, Antiphospholipid Sx or renal disease
• NB: risk is ↓ in smokers.
IUGR, Hydatiform mole, multiple pregnancy and foetal hydrops.
Management of Hypertension in Pregnancy
1. Identify those at risk
a) Preventative measures
2. Treatment of pre-existing HTN
3. Treatment of Mild HTN
a) Lab monitoring
b) Foetus monitoring
c) Conservative therapy
4. Treatment of severe pre-eclampsia
a) Initial management
b) Correction of HTN
c) Rx of seizures
1. Identify those at risk
a) Preventative measures
Antenatal BP checks, urinalysis
May consider MgSO4 prophylaxis in risk++
Uterine artery Doppler US may identify high risk women – consider aspirin
? Fish oil
2. Treatment of pre-existing HTN
Usually BP >140/90 preconception or before 20wks ± strong FHx
Does ↑ risk 5x of pre-eclampsia, placental abruption, IUGR
Mx – methyldopa or labetalol + regular maternal/foetal monitoring.
o Don’t use ACEi, diuretics, propanolol (teratogenic)
3. Treatment of Mild HTN
Admit if BP ≥160/100 or ≥140/90 + proteinuria or IUGR
a) Maternal monitoring
BP q2-4 hrly
Daily weights + fluid balance
FBC, EUC, Uric acid, LFTs, Coags, UA + M/C/S
b) Foetus monitoring
Do serial CTG and US
c) Conservative therapy
May just monitor
May elect to treat with labetalol/methyldopa to buy time
NB: delivery is the only cure (give H2 blockers at onset of labour)
4. Treatment of severe pre-eclampsia
a) Initial management
Confirm Dx
o BP > 160/110 + 0.3g proteinuria
Cameron Korb-Wells & Kai Brown (2009)
BP ≥140/90 + proteinuria +
 Seizures
 H/A or epigastric pain
 Plts <100
 Visual disturbance
 Creat. >100umol/L (or CrCl <80mL/L)
 ALT > 50
 Clonus
Get expert O&G and anaesthetics help
Monitor vitals and BP q15min
MgSO4 4g IV over 15min
IV fluids restricted to 85ml/hr + Catheterise to monitor UO
FBC, UEC, LFTs q12hrs
Foetal CTG, Doppler and US
b) Correction of HTN
If very high….160>110
o Hydralazine 5mg IV slowly unless pulse >120bpm
 Repeat q20min until 20mg max.
o May also use nifedipine (also tocolytic) or labetalol.
o May consider IV albumin if oliguric, may use mannitol or 20mg IV
frusemide if overloaded.
c) Rx of seizures
Most fits occur >48hrs post-partum. Continue monitoring until clinically and
biochemically normal.
1 seizure
o 4g MgSO4 in 100ml NS over 5min + 1g/hr infusion for 24hrs.
 Beware ↓ resp.
Recurrent Seizures
o 2g MgSO4 bolus
o Check resp. rate (stop infusion if RR<14 or SaO2 <95%) and
tendon reflexes q15min
o Have Calcium gluconate ready in case of MgSO4 toxicity.
o May consider diazepam at consultants discretion
o May consider CT head if fits continue.
o Do not use ergotamine (↑ risk stroke), use oxytocin.
NB: pre-eclampsia behaves unpredictably, BP may not be a good marker. Proteinuria of even
1+ may be significant. Antihypertensives only aim to prevent stroke, not cure. Diuretics
usually contraindicated as most patients are intravascularly depleted.
meticulous control around conception ↓ malformation rates
some glycosuria is normal (↑ filtration, ↓reabsorption)
 Maternal
 20% pre-existing DM develop proliferative retinopathy – screen x2
 Hyramnios (25% - ?foetal polyuria)
 Preterm labour
 Stillbirth near term
Cameron Korb-Wells & Kai Brown (2009)
 3-4x risk malformation
o Rarely, sacral agenesis (almost exclusive to DM mothers)
 Macrosomic or IUGR
 Hypoglycaemia
 ↓ Ca , ↓ Mg
 Polycythaemia (29%) - ↑ risk neonatal jaundice.
1. Prenatal care
a. Optimisation and education
2. Antenatal care
a. Monitoring BSL and complications
3. During Labour
a. Be aware of complications
b. Insulin and dextrose drip
4. Postpartum care
a. Cease hypoglycaemic meds temporarily
b. If breastfed – insulin, otherwise orals OK
c. Monitor follow up BSLs and neonatal complications
Prenatal care
a. Optimisation and education
Optimise glycaemic control
Education on risks and complications
Advice preconception folic acid 5mg daily
Evaluate for end-organ disease
2. Antenatal care
a. Monitoring BSL and complications
Refer to diabetes clinc
Confirm dates, morphology scan at 20wks (± echo at 22wks if early control
Monitor HbA1c (although tends to be falsely low due to dilution) and BSL
o Aim for fasting BSL <5mmol/L, 1hr post-prandial <8mmol/L
o Insulin requirements ↑ 50-100% as pregnancy progresses.
o Give glucagon kit and ensure partner knows how to use it.
For type-II DM, generally cease all meds and aim for lifestyle control, else
o NB: oral hypoglycaemics CI except for glyburide that does not
cross the placenta (may be safe)
3. During Labour
a. Be aware of complications
Aim for delivery between 36-38 weeks to avoid stillbirth/macrosomia, or
closer to term at specialised centres to ↓ risk RDS.
Avoid acidosis and monitor foetus, avoid maternal hyperglycaemia (causes
foetal hypoglycaemia) esp. in b-sympathmomimetics or steroids are used.
Beware shoulder dystocia with big babies My consider LSCS.
Clamp cord early as polycythemia risk.
Cameron Korb-Wells & Kai Brown (2009)
b. Insulin and dextrose drip
Give 1L 5-10% glucose 8hrly IVI with 1-2U insulin/hr via pump.
4. Postpartum care
a. Cease hypoglycaemic meds temporarily
Insulin needs fall dramatically post-partum with expulsion of the placenta.
o Monitor BSL, may not need any insulin for ~48hrs
o Restart at pre-pregnancy dosage.
b. Encourage breastfeeding (↓ insulin requirement)
c. Monitor follow up BSLs and neonatal complications
Gestational Diabetes
Dx on OGTT ≥8mmol/L at 2hrs
Incidence 3%
Up to 50% will get DM later in life
Early phase of pregnancy is anabolic (↑ insulin), letter phase is catabolic (↑
human placental lactogen and cortisol ↑ insulin resitance)
Risk factors
o Age > 30yrs
o 1 degree relative with DM
o Unexplained stillbirth
o Prior GDM
o Mothers who themselves were low birth weights or IUGR
o Usually can be managed by close monitoring with a BSL diary,
exercise and dietary intervention
 Avoid smoking
o Occasionally insulin is required.
o Follow up OGTT 6-12 weeks post-partum, yearly fasting BSL +
lifestyle advice.
Most common medical complication of pregnancy
Increased risk in pregnancy due to urinary retention (progesterone stasis)
Minimise risk by maintaining high fluid intake, complete emptying of bladder.
Asymptomatic bacteriuria in 2-7% of pregnant women
 25% will get pyelonephritis
 Increased risk PROM/preterm labour
 UA (nitrites, WBC, RBC)
 Urine M/C/S
 Cystoscopy, UEC, FBC in severe/recurrent infections
 Treat all women with asymptomatic bacteruria to prevent PROM and preterm
 Cephalexin 500mg OD PO for 10 days
Cameron Korb-Wells & Kai Brown (2009)
o Nitrofuantoin or augmentin alternatively.
o Admit for IV antibiotics if pyelonephritis is suspected.
Repeat culture at least 48hrs after cessation of treatment.
Defined as vomiting that results in weight loss (>15% body mass)
1% incidence (↑ young mums, non-smokers, molar pregnancy)
May result in…
o nutritional deficiency,
o dehydration,
o tachycardia,
o electrolyte disturbance,
o polyneuritis (↓ vit B),
o renal and liver failure
Examination for level of dehydration
Psychological support
a) Rehydrate
b) VTE prophylaxis
c) Anti-emetics
d) Parental nutrition
Examination / Investigations
• BP (lying and standing)
• Chart weight (losses)
• FBC, UEC, LFT (50% have abnormal LFTs), TFTs (60% abnormal – biochemical
hyperthyroidism, but clinically normal)
• Urine M/C/S
• Admit
• Psychological wellbeing
• Most settle with time
o Rest, small meals, moreso carbs, lightly carbonated drinks
• Routine thiamine (prevent Wernicke’s – 40% foetal loss)
• Severe:
o Correct dehydration IV
o Give thromboprophylaxis
o May give metaclopromide or ondansetron…steroids as a second line
o Parenteral nutrition may rarely be needed.
Consult expert help
During labour avoid lithotomy position (↓ venous return), aim for short second stage
Monitor for heart failure – have O2 and cardiac drugs ready
Cameron Korb-Wells & Kai Brown (2009)
Hyperthyroidism in pregnancy
o ↑ risk prematurity, malformations and foetal loss
o TSH abs cause foetal hyperthyroidism – risk difficult delivery.
o Labour may precipitate thyroid storm
o Rx – carbimazole or propylthiouracil, partial thyroidectomy in 2 trimester,
regular monitoring.
 Neonatal Grave’s (1% in mother’s with Grave’s)
• Crssing of TSH abs
o ↑ rates of miscarriage, stillbirth and prematurity.
o Optimise T4 preconception, and adjust according to monitoring (req. usually
Postpartum thyroiditis (up to 5% prevalence)
o Hyper then hypo (~4 mo post-partum)
o Symptomatic Rx, anti-thyroid drugs ineffective (destruction releasing
thyroxine, not stimulation).
Get expert help
Intrahepatic cholestasis of pregnancy (0.5-1.5% of all pregnancies)
o Presents with pruritis in 2 trimester.
o Must exclude viral hepatitis
o Risk preterm labour, foetal distress and stillbirth – aim for delivery at 38wks
o Give Vit K to mother and baby at birth
Acute Fatty Liver of Pregnancy
o Rare but grave.
o ABdo pain, jaundice, headache, vomiting ± thrombocytopenia + pancreatitis.
o Associated with pre-eclampsia
o Usually occurs after 30wks
o Treatment is supportive and deliver soon
Exacerbations increase in pregnancy and puerperium
Most are mild-mod
Increased risk pre-eclampsia
Pregnancy should be ideally planned, aspirin should be used throughout.
Foetus rarely affected by Abs (either self-limiting rash on face or congenital heart block)
Rx – steroids
d) Maternity "blues"
e) Antenatal and Post-natal depression (PND)
f) Post-partum psychosis
Childbirth & Becoming a Parent requires the capacity for rapid & massive
psychological adjustment
Maternity ‘blues’
• A benign condition: 50-60%.
Cameron Korb-Wells & Kai Brown (2009)
Sx peak b/n 3rd-5th day and gone by 10th day.
Mood lability: elation (days 1-2), irritability, anxiety, depressed, poor concentration.
Up to 30% go on to subsequent PND (severe cases)
Treatment: reassure but be aware it may be early stages of PND
Perinatal Depression
• Increasing evidence that prevalence of “depression” similar in pregnancy &
• Incidence postnatal anxiety disorder 10%
 refocus on Perinatal mood & anxiety disorder
Clinically no different to other depressions but :
a) need to differentiate from adjustment to childbirth (50% depression undetected by GP's &
b) major consequences for mother, infant and family
c) crucial that 10 care workers detect as more likely to be acceptable as first line intervention
13% prevalence (O’Hara 1996)
3x higher rate of new onsets within 5 weeks of childbirth cf. matched control group
greatest risk of depression than any other time in woman's life.
• 50% in 1st 3 months
• often not diagnosed till much later
Risk Factors:
1. Biological
• Hormonal factors: significant for a subgroup of women
• Past history of PND, or affective disorder: 2-4 x risk of subsequent PND
• family history affective illness
2. Psychosocial
• mother's own negative experience of parenting
• ambivalence about pregnancy
• Personality, low self-esteem, negative cognitions.
• recent life events
• Obstetric/perinatal difficulties
• past TOP, miscarriage:
• Poor social supports
• marital/family probs
Clinical presentation
Detection can be confounded by:
• "unsettled" baby
• disturbed sleep/anxiety seen as normal in this context
• tendency to downplay symptoms as "normal"
• focus on physical aspects of p-p
• mood: depressed, irritable, anxious, labile
• panic attacks
• sleep: reduced in spite of baby sleeping
• appetite: variable
• libido: fails to recover
• lack of pleasure in baby, other activities
• poor "bonding"
• social withdrawal
• marital problems
• undue concern for baby's health
• "unworthy" mother
Cameron Korb-Wells & Kai Brown (2009)
obssessional features
suicidal/infanticidal ideation
1. Mother
• untreated, 50%-70% remain depressed 6 months later
• 25% go on to chronic/unremitting course (Watson 1984)
• 25% go on to recurrent depression
• ↓ social, emotional, cognitive and behavioural development of infant
• mother-infant attachment may be impaired: if severe, poor parenting style and
personality problems may be seen in adulthood
3. Partner, family, community
• divorce > disintegration of the family unit and the high psychological costs of
single parenthood.
• public cost: welfare, judicial, and psychiatric services
Post-partum Psychosis
Incidence: 1-2/1,000
Onset: 75% within 2-3 weeks
Diagnostically not a single entity
Risk Factors:
• Primiparity
• past hx.
Clinical features (Affective type):
• rapid onset
• depressed or manic (mixed)
• perplexity and confusion
• mood-congruent psychotic features
• complete recovery for index episode
• subsequent puerperal psychosis:
o 50-100% (nb. within 2 yrs)
o lifetime recurrence: unipolar depression 60-80%
o bipolar/szia (80%)
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to understand the
changes in anatomy, physiology and psychology that occur in pregnancy so
that they appreciate the principles of management of labour; know how to
supervise a spontaneous delivery.
Anatomy of the female pelvis and fetus relevant to labour and delivery
Pelvis has four imaginary planes:
o 1 - plane of the pelvic inlet,
o 2 - plane of greatest pelvic dimensions,
o 3 - plane of the midpelvis (least pelvic dimensions),
o 4 - plane of the pelvic outlet.
Pelvic inlet bounded posteriorly by the promontory, laterally by the linea terminaiis,
and anteriorly by the horizontal rami of the pubic bones and symphysis pubis
Four diameters of pelvic inlet are described
o Anterposterior (11cm)
o Transverse (13cm)
o Two obliques (12 cm from left or right sacroiliac synchondroses to the
iliopectineai eminence on the opposite side of the pelvis)
Plane of greatest pelvic dimension extends from the middle of the posterior surface of
the symphysis pubis through the ischial bones over the middle of the acetabulum to
the junction of second and third sacral vertebrae. Its anteroposterior and transverse
diameters are 12,5 cm.
Midpelvis at level of ischial spines is particular importance following
engagement of the fetal head in obstructed labor. The transverse diameter
(interspinous) is 10,5 cm and anteroposterior is 11cm.
Pelvic outlet has two diameters: anteroposterior extends from the lower margin of the
symphysis pubis to the tip of the coccyx (9,5cm) and transverse diameter between
the inner edges of the ischial tuberosities 11.5 cm.
Cardinal movements of labour
• Engagement
• Descent
• Flexion
• Internal Rotation (to OA position ideally)
• Extension (delivery of head)
• External Rotation (restitution); head rotates in line with the shoulders
• Expulsion (delivery of shoulders and body)
Cameron Korb-Wells & Kai Brown (2009)
Assist conduct of normal labours and deliveries
Clinical procedures in normal labor/delivery
Obstetric examination: aim to assess fetal lie (Leopold maneuvers  palpate
fundus in maternal abdominal quadrants, then either side of uterus, then presenting
part over symphysis), determine fetal presentation (breech or cephalic) and
engagement (fifths above), station
o Station: refers to position of presenting part relative to ischial spines
Cameron Korb-Wells & Kai Brown (2009)
 at ischial spines = station 0 = engaged
 2 cm below ischial spines = station +2
Rupture of membranes: PROM >18 hours prior to labor, PPROM <37 weeks;
diagnosis suspected with history of gush/ leaking fluid from vagina, though may be
difficult to distinguish stress incontinence and small amounts
o Nitrazine test (amniotic fluid alkaline cf acidic vaginal secretions)
o Fern test (oestrogens crystalise salts in amiotic fluid upon drying – though
caution cervical mucous also ferns)
o Amnisure (molecular test identifying placental alpha-microglobulin-1 by
o U/S examination: if fluid previously normal and no reason to suspect low
fluid, oligohydramnios is indicative
o Amniocentesis (amnio dye test/ tampon test): inject dilute indigo carmine
dye to look for leakage from cervix
Cervical examination: dilation, effacement, fetal station, cervical position,
consistency of cervix  Bishop score (≥8 favourable for labor)
Fetal presentation/position: presentation may be cephalic/ breech/ transverse
o Cephalic: vertex, face, brow or compound (with limb)
o Breech: frank, complete or footling
o Fetal position: determined by palpating sutures and fontanelles, abnormal
include OT/OP  prolonged labor and higher rate C/S
Diagnosis of labor: regular uterine contractions causing cervical change
Stages of normal labor/delivery
• Begins at onset of regular contractions producing cervical dilatation
• Ends at full cervical dilatation @ 10cm
• Duration
o Nulliparous 6-18 hours
o Multiparous 6-8 hours
• Latent phase: infrequent/ irregular contractions, slow cervical dilatation (to 3-4cm
and effacement)
• Active phase: rapid dilatation to full dilatation, rate 1.2cm/h nulliparous, 1.5cm/h
multiparous  phase of maximum slope on Friedman curve
• Difficulties in first stage:
o Think of the 3 P’s!
 Power: strength and frequency of uterine contractions
 Passenger: fetal size, lie, presentation
 Pelvis: pelvic size
o If rate of dilatation <5 centile (1cm/hr), consider three P’s to assess whether
vaginal delivery can be expected. If no change in dilatation or station for 2
hours with adequate uterine contractions, deemed active phase arrest 
common indication for C/S
• Begins full cervical dilatation
• Ends delivery of infant
• Duration
o Nulliparous 2 hours (3 hours epidural)
o Multiparous 1 hour (2 hours epidural)  rare to last >30 minutes unless fetal
macrosomia, persistent OP or OT position
• Operative vaginal delivery: forceps or vacuum-assisted, where prolonged second
stage, maternal exhaustion or need to hasten delivery. Decision between the two
usually based on clinician preference and experience.
o Forceps: blades around fetal head, operator using leverage on handles to
aid maternal expulsion efforts. Require full dilatation of cervix, ruptured
membranes, engaged head and at least 2+ station, no CPD, adequate
anaesthesia, empty bladder.
Cameron Korb-Wells & Kai Brown (2009)
Complications: facial/head bruising, lacerations to fetal
head/cervix/vagina/perineum, facial nerve palsy, skull #/ intracranial
Vacuum: safe conditions identical to forceps, exertion on fetal scalp made
parallel to axis of maternal pelvis with maternal bearing-down and uterine
 Complications: scalp laceration, cephalohematoma, rarely subgaleal
haemorrhage (neonatal emergency)
THIRD STAGE (conduct, examine placenta/ cord/ membranes)
• Begins delivery of infant
• Ends separation and expulsion of the placenta
• Duration: up to 30 minutes before intervention indicated
• Signs of placenta separation: gush of blood, lengthening of cord, uterus becomes
globular and fundus rises  no attempt should be made to deliver placenta until all
these signs noted
• Placental delivery: syntocinon IM at delivery of posterior shoulder, controlled cord
• Retained placenta: if placenta does not deliver within 30 minutes after infant.
Common in preterm deliveries, particularly previable, though ALSO sign of placenta
accreta where placenta invaded into or beyond endometrial stroma
o Manual extraction: hand in intrauterine cavity, using fingers to shear
placenta from uterine surface
o Curettage: if cannot be extracted manually, to ensure no POC remain
Placental separation and drugs affecting uterine muscle activity
• Background
o Phys: placenta separates as a result of shearing force between the placental
surface and the uterine wall in the presence of uterine muscular contraction
o Degree of blood loss with placental separation and delivery depends on
how efficiently the placenta separates from the wall, how effectively the
uterine muscle contracts around the placental blood vessels and how quickly
the placenta is expelled from the uterus, through the cervix and birth canal
o Management of third stage can directly influence important maternal
outcomes including need for manual removal of placenta and incidence of
 May be either “Expectant” or “Active” – active is recommended.
Expectant cannot be recommended on the basis of evidence
• Active management: oxytocic administration followed by assisted delivery of the
o Oxytocic administration
 Timing: oxytocic with delivery of anterior shoulder may maximise
benefit in terms of preventing PPH. Caution must be exercised if
possibility of undiagnosed second twin (i.e. no ultrasound in
Cameron Korb-Wells & Kai Brown (2009)
Agents: number of oxytocic regimens, most popular oxytocin 5 or 10
units intravenously OR Syntometrine 1ml intramuscularly
(ergometrine 0.5 mg + oxytocin 5 units) OR oxytocin 10 units
 Disadvantages: ergometrine  nausea and vomiting and may lead to
raised blood pressure (IM ergometrine  milder S/E). Slight increase
in incidence of manual removal of placenta with active management
of the third stage of labour
o Assist delivery of the placenta: essential to ensure uterus well contracted
and placenta separated before controlled cord traction is applied
Expectant management
o Await spontaneous contraction of uterus, separation of placenta and delivery
of placenta and membranes
o Measures such as nipple stimulation or postural changes may be employed
o Expectant management associated with ~2x increase in PPH and increased
risk of blood transfusion when compared with active. Poorly contracted uterus
poses increased risk of the potentially fatal complication of uterine inversion
o Facilities must be immediately available to treat postpartum haemorrhage
Pain relief (pharm and other) and effects on fetus and mother
Epidural (bolus, more can be infused)
o L3/4 region (anaesthatises T11-S5 pain fibres)
o Setup IV line + give 500ml IV Hartmans 1 to prevent BP drop
o Check PR, BP, Resps, contractions, fetal hr every 15mins
o Requires 2 hourly top ups
o Helpful for: OP position, breech, multiple gestation, preterm delivery, preeclampsia, forceps, inco-ordinated uterine contractions.
o Problems:
 Slows active phase of labor
 Postural hypotension
 Urinary retention
 Paralysis
 Post delivery: urinary retention + headache
o Can be loused if need to go to C/S
Spinal (one off dose)
o More common for C/S
Nitrous oxide
o +ve:
 use throughout labour
 patient initiated/administered
o C/I: pneumothorax
o Useful to relax 1 stage
o Cross placenta so shouldn’t be used within 2-3hrs of delivery (though can use
naloxone to reverse so long as mum is not narcotic dependant!)
o Analgesia onset in 20 min with duration 2-3 hours
o Low doses may produce vomiting without pain relief (give enough!)
o Other S/E: disorientation, decreased gastric emptying, neonatal respiratory
o C/I: mum on MAO-I’s
o For episiotomy
o For C/S, esp emergent
Pudendal block
o Injected:
 where pudendal nerve travels just posterior to the ischial spine at its
juncture with the sacrospinal ligament
Cameron Korb-Wells & Kai Brown (2009)
Or: 1cm beyond a point just below and medial to the ischial spine on
each side.
Commonly used with forceps or vacuum delivery.
Intrapartum fetal monitoring
Management of a spontaneous breech
• Definitions
o Complete: flexion at hips and knees
o Frank: flexion at hips, extension at knees (most common type, also most
common to be delivered vaginally)
o Footling: may be single or double with extension at hip(s) and knee(s) so
that foot is the presenting part
Cameron Korb-Wells & Kai Brown (2009)
Epidemiology: occurs 3-4% of pregnancies at term (25% before 28 weeks)
Risk factors
o Maternal risk factors: pelvis (contracted), uterus (shape abnormalities,
intrauterine tumours, fibroids, extrauterine tumours causing compression),
grand multiparity
o Materno-fetal: placenta (previa), amniotic fluid (poly/oligohydramnios)
o Fetal: prematurity , multiple gestation, congenital malformations (6% of
breeches; 2-3x the incidence in vertex presentations)
Presentation: noted by Leopold manoeuvres and U/S
External version
o Criteria: > 37 weeks, singleton, unengaged, reactive NST
o C/I: previous T3 bleed, prior classical C/S, previous myomectomy,
oligohydramnios, PROM, placenta previa, abnormal U/S, suspected IUGR,
hypertension, uteroplacental insufficiency
o Risks: abruption, cord compression
o Method: tocometry, salbutamol IV monitoring maternal tachy, followed by
ultrasound guided transabdominal manipulation of fetus
 If patient Rh negative, give anti-D prior to procedure
o Good prognostic factors (for a successful version)
 Multiparous
 Good fluid volume
 Small baby
 Skilled obstetrician
Criteria for vaginal delivery
o Frank or complete breech, GA > 36 weeks
o Estimated birth weight 2500-3800g
o Fetal head flexed
o Continuous fetal monitoring
o Maternal pelvis adequately large (clinically, or “proven” by delivery)
o No other indication for C/S
C/S for all other presentations
o Recommended if breech not descended to perineum in second stage after
two hours, in absence of active pushing, or if vaginal delivery not imminent
after one hour of active pushing
o Recent study: For women with frank or complete breech presentations,
perinatal mortality, neonatal mortality, and serious neonatal morbidity is
significantly lower for those with planned C/S over those with planned vaginal
birth, with no significant difference in maternal complications
Episiotomy (indications and technique, principles of repair)
Episiotomy: incision made in perineum to facilitate delivery
o Hasten delivery
o Shoulder dystocia
Once cut, great precaution to support perineum around wound to avoid extension 
episiotomy associated with more severe tears
Laceration repair: usually after placenta delivery
o Thorough examination to assess lacerations: perineum, labia, periurethral
area, vagina, anus and cervix, as well as PR exam to assess for “button-hole”
fourth degree laceration
o First degree: mucosa, skin
o Second degree: extend to perineal body but not anal sphincter
 Technique: apex of laceration (often lying beyond hymenal ring)
located and suture anchored at apex, then run down to level of
hymenal ring to bring together vaginal tissue, passing beyond
hymenal ring to bring together perineal body. Separate suture may
be used to place a “crown stitch” brining together the perineal body.
Skin of perineum closed with subcuticular closure
Cameron Korb-Wells & Kai Brown (2009)
Third degree: into or completely through anal sphincter
 Technique: repair anal sphincter with several interrupted sutures,
then rest of repair as second degree
Fourth degree: anal mucosa entered
 Technique: repair anal mucosa first, meticulously to prevent fistula
formation, then repair as third degree
Apgar score and relevance
Active resuscitation of the newborn (indications and dangers)
High risk deliveries
 Preterm infants < 35 weeks gestation
 Multiple births
 Infants with significant congenital malformation diagnosed antenatally
 Abnormal CTG or scalp pH < 7.20
 Thick (particulate) meconium stained liquor
 Breech delivery
 Instrumental delivery (not uncomplicated low forceps or vacuum lift-out)
 Caesarean section under general anaesthetic
 Emergency caesarean section
 Opioids administered to the mother within 4 hours of delivery
 Other situations where there is concern of infant compromise
Cameron Korb-Wells & Kai Brown (2009)
Initial Resuscitation
 Anticipation - know maternal history, history of pregnancy, labour, and delivery for
all infants (“before ABC’s”)
o Prevent heat loss by drying, warming (on radiant heater, remove wet towels)
o Position head and neck to open airway for suction
o Stimulate infant by rubbing back or slapping foot
 Airway
o Gentle suction of mouth then nose
o With thick meconium, suction nasopharynx as head is delivered, then
consider intubation and suction of trachea
 Breathing
o Check for spontaneous respirations
o Bag and mask if apneic/gasping/HR < 100/min, bag at a rate of 40-60/min
with 100% O
o Intubation is indicated if: prolonged ventilation required, bag and mask not
effective, tracheal suctioning is needed (thick meconium), HR remains <
100/min, diaphragmatic hernia is suspected (do NOT bag)
 Circulation
o Bradycardia is usually due to hypoxia from respiratory arrest and responds to
ventilation with 100% O2
o "80 or less compress" - if bradycardic (apex < 80/min and no improvement
with bagging) or asystolic, compressions begin at rate of 120/min
o Coordinate 3 compressions with 1 ventilation (120 compressions/min, 40
 Check after 30 seconds
 If HR > 80 stop compressions but continue ventilation until HR >100
 Drugs
o Epinephrine - for asystole or severe bradycardia
o HCO 3 (4.2% solution given slowly) -for documented acidosis or prolonged
o CaCO 3 - may be indicated for continued circulatory failure
o Narcan - if mother given narcotics in labour
Routine neonatal care
 Vitamin K (IM) - to avoid hemorrhagic disease of newborn
 Screening tests
o All neonates: PKU, TSH usually after 24 hours of life
o If mother Rh negative: blood group, direct antiglobulin test
o If indicated: sickle cell, G6PD deficiency
 If mother Hep B positive: HBIG and start Hep B vaccine series
Cameron Korb-Wells & Kai Brown (2009)
Cameron Korb-Wells & Kai Brown (2009)
1. Demonstrate a complete knowledge of the components of a
partogram. Students should be able to interpret the partogram in order
to recognise deviations from normal labour and its use in preventing
prolonged labour.
2. Discuss the meaning of trial of labour
3. Identify signs that may indicate fetal distress and discuss their causes
and implications for the future
4. Discuss normal and abnormal uterine action
5. Have knowledge of the effects of prolonged labour on mother and
Partogram - cervical dilation, fetal heart rate/CTG, duration of labour, vital signs and
Cervical dilatation/Effacement
latent phase
 uterine contractions typically infrequent and irregular
 slow cervical dilatation (usually to 3-4 cm) and effacement
active phase
 rapid cervical dilatation to full dilatation
o (nulliparous ~1 cm/h and ~1.5 cm/h in multiparous)
 phase of maximum slope on Friedman curve (see Figure 6)
 painful, regular contractions ~q2 min, lasting 45-60 seconds
 contractions strongest at fundus, weakest at lower segment
First Stage: 6-18hr in nulliparous (2-10 in multip)
Second Stage: 30min-3hrs in nulliparous (5-10min in multip)
Third Stage: should not last >30min before intervention.
Trial of Labour
 Attempting vaginal delivery after previous caesarean
 Generally safer than automatic repeat caesarean (less so if labour is induced)
Foetal Distress – signifies hypoxia
 Persistent tachy or brady
Late decelerations on CTG
 Low variability
 Low pH (deliver urgently if <7.24)
 Meconium stained liquor
o in general, meconium may be present in up to 25% of all labours;
o usually NOT associated with poor outcome, but extra care is required at time
of delivery to avoid aspiration and RDS
Cameron Korb-Wells & Kai Brown (2009)
Predisposing Factors
• Previous twins
• Increasing maternal age
• Early pregnancy
• Uterus too large for dates
• >2 poles may be felt, >1 foetal heart rates
• Dx confirmed on U/S
o Mono or dicorionic
• Pregnancy
o Polyhydramnios
o Pre-eclampsia
o Anaemia
o APH (abruption and praevia)
• Foetal
o Perinatal mortality
o Prematurity
o Malformation rates x2-4
o Monozygotic twins – risk twin-twin transfusion syndrome
• Labour
o Malpresentation
o Rupture of vasa praevia
o Cord prolapse
• Ensure adequate rest
• U/S for diagnosis and more regular follow ups on foetal growth
• Additional iron and folate
• More antenatal visits (↑ risk pre-eclampsia)
• Educate mother on identification of preterm labour
• Consider induction at 40 weeks
o IV running at labour
o Anaesthetist on hand
o Paediatrician x2
6. Discuss the initial management of transverse lie, cord prolapse, and
shoulder dystocia.
7. List the common indications for and the complications of Caesarean
8. List the common indications for and complications of forceps delivery /
 Maternal factors
o pregnancy-induced hypertension
Cameron Korb-Wells & Kai Brown (2009)
o maternal medical problems, e.g. diabetes, renal or lung disease
Maternal-fetal factors
o Rh isoimmunization
o chorioamnionitis
o post-term pregnancy
Fetal factors
o suspected fetal jeopardy as evidenced by biochemical or biophysical
o fetal demise
 Maternal
o prior classical incision or complete transection of the uterus
o unstable maternal condition
o gross cephalopelvic diameter (CPD)
o active maternal genital herpes
 Maternal-fetal
o placenta or vasa previa
 Foetal
o distress
o malpresentation
o preterm fetus without lung maturity
Prerequisites for Labour Induction
 Maternal
o short anterior cervix with open os (“inducible" or “ripe”)
o if cervix is not ripe, use prostaglandin (PG) gel (see below)
 Foetal
o adequate fetal monitoring available
o cephalic presentation
o good fetal health
 Likelihood of success determined by Bishop Score (cervical characteristics)
o score of 9-13 associated with high likelihood of vaginal deliver
 descent of the cord to a level adjacent to or below the presenting part causing cord
compression between presenting part and pelvis
 increased incidence with prematurity/PROM, fetal malpresentations, low-lying
placenta, polyhydramnios, multiple gestation, CPD
 visible or palpable cord
 FHR changes (variable decelerations, bradycardia or both)
 emergent C/S
 adjunctive measures
o alleviate pressure of the presenting part on the cord
o keep cord warm and moist by replacing it into the vagina and/or applying
warm saline soaks
Cameron Korb-Wells & Kai Brown (2009)
impaction of anterior shoulder of fetus against symphysis pubis after fetal head has
been delivered (life threatening emergency)
Risk factors
 maternal
o maternal obesity
o diabetes
o multiparity
 fetal
o prolonged gestation
o macrosomia
 labour
o prolonged 1st and 2nd stages
o prolonged deceleration phase (8-10 cm)
o instrumental midpelvic delivery
 watch for “turtle sign” (head advances during contraction but returns to previous
position at end of contraction)
 chest compression by vagina or cord compression by pelvis can lead to hypoxia
 danger of brachial plexus injury (Erb palsy)
 fetal fracture (clavicle, humerus, cervical spine)
 maternal perineal injury, may result in PPH
 goal: to displace anterior shoulder from behind symphysis pubis; follow a stepwise
approach of maneuvers until goal achieved
A: apply suprapubic pressure
A: ask for help
L: legs in full flexion (McRobert’s maneuver)
A: anterior shoulder disimpaction
R: release posterior shoulder
M: maneuver of Wood’s corkscrew
E: episiotomy
Other (last resort)
o cleidotomy: deliberate fracture of the clavicle
o Zavanelli maneuver: replacement of fetus into uterine cavity and emergent
 used when there is a delay in the second stage
o ↓ maternal effort, epidural anaesthesia, malposition of foetal head
 used in assisted breech delivery
 used in assisted delivery of preterm infant
 Assisted delivery with face presentation
 Assisted delivery with coagulopathy
 Assisted delivery in cord prolapse.
 Complications
o maternal: anesthesia risk, lacerations, injury to bladder, uterus, bone, pelvic
nerve damage, PPH, infections
o fetal: fractures, facial nerve palsy, trauma to face/scalp,
intracerebralhemorrhage (ICH), cephalohematoma, cord compression
Cameron Korb-Wells & Kai Brown (2009)
rotation occurs naturally
can be inserted through a partially dilated cervix
CI in face or breech presentations
Haematoma (‘chignon’) resolves in 2 days.
o May predispose to neonatal jaundice
o Subgaleal haemorrage may look like chignon but haematoma spreads across
whole skull over hours – may result in haemorrhage and shock.
Maternal morbidity is higher than vaginal delivery – infection, ileus, VTE
 Failure to progress, foetal distress, cord prolapse
 Breech
 Previous caesarean
 Placenta praevia
 Some maternal infections e.g. Herpes or HIV
 Other maternal medical complicaitons
infection (UTI, wound, endometritis)
injury to surrounding structures
thromboembolic phenomena
increased recovery time/hospital stay
Cameron Korb-Wells & Kai Brown (2009)
9. Discuss the cause, diagnosis and appropriate emergency management
of a post partum haemorrhage
10. List the causes of shock during labour and early puerperium and
indicate the emergency management of these patients
11. Discuss the causes of intra partum haemorrhage
12. Have knowledge of the causes and management of intra-partum
PPH – loss >500mL in first 24hrs (occurs in 6%). Major PPH >1L occurs in just >1%
 Uterine atony
 Retained placental tissue
 Full bladder
 Prolonged labour
 Forceps or other traumatic delivery
 Grand multiparity
 Twins and polyhydramnios (causing over distension of the uterus)
 Antepartum haemorrhage
 Anaesthesia
 Relaxant drugs
 Genital tract trauma
 Clotting disorders
Risk Factors
 Past Hx atony with PPH
 Retained placenta
 Ether or halothane anaesthesia
 Large placental site (twins, severe rhesus disease, large baby)
 Low placenta
 Overdistended uterus (large baby, polyhydramnios)
 Placental abruption
 Uterine malformations or fibroids
 Prolonged labour
 Older mothers.
Obstetric Shock
 Assoc. with…
o abruption,
o placenta praevia,
o ruptured uterus (usually in labour, pain variable, intraabdominal bleeding,
sudden unexplained shock, disappearance of presenting part, cessation of
o inverted uterus (bleeding variable, rapid shock > blood loss due to autonomic
response – Mx: manual or fluid reduction + ABx),
o amniotic fluid embolus – resus ± ionotropes
o PE
o Adrenal haemorrhage
o Septicaemia
 Complication can include Sheehan Syndrome (pituitary necrosis)
o ↓ TSH - hypothyroidism
o ↓ ACTH – Addision’s disease
o ↓ LH / FSH – genital atrophy.
Cameron Korb-Wells & Kai Brown (2009)
Management of PPH
ABC + monitoring
Ergotamine IMI + set up syntocin drip
Get help
Treat shock
Is there uterine atony? placenta delivered?
Is there trauma to the birth canal?
Further measures
a. Prostaglandin
b.Surgical haemostasis
1. ABC + monitoring
ABC + high flow O2 and fluids
2. Ergotamine IMI + set up syntocin drip
0.25mg ergotamine (except in HTN)
Add 40U oxytocin to 1L Ringer’s lactate/Hartmann’s
3. Get help
Anaesthetist + experienced O&G
4. Treat shock
NS, colloid or matched whole blood if possible
Aim for sBP >100, UO >30ml/hr
5. Is there uterine atony? placenta delivered?
Uterine atony
 Bulk, soft
 Should massage fundus to induce contractions + haemostasis.
 If not – removed under GA
 If it is, examine the placenta to ensure it is complete (lobes and
 May apply gentle traction on cord.
6. Is there trauma to the birth canal?
Lithotomy positions, good analgesia and lighting
7. Investigations
Prob already know corssmatrch
Check blood clotting at bedside
 5ml should take <6min to clot in round-bottomed glass tube
Send FBC, UEC, LFT, Coags, D-dimer
9. Further measures
a. Prostaglandin F2-alpha
 Give via IV, IMI or intrauterine myometrium.
 Can give repeated doses, stops bleeding in 88%
Cameron Korb-Wells & Kai Brown (2009)
b. Surgical haemostasis
 Brace uterine suture
 Vessel ligation
 Vessel embolisation
 Hysterectomy
13. Understand the emotional effects of an unexpected pregnancy
outcome on the family
Guilt, self-blame, bereavement
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to understand the aetiology, pathology
and clinical manifestations of miscarriage, ectopic pregnancy and of trophoblastic diseases so
that such conditions can be identified and appropriate management instituted.
Miscarriage (types and how to differentiate one from the other)
Spontaneous abortions are estimated to occur in 15-25% of all pregnancies, with number
potentially even higher as losses between 4-6 weeks gestational age often mistaken for late
• Spontaneous abortion/ miscarriage: pregnancy ending before 20 weeks
• Abortus: fetus lost <20 weeks, <500g or <25cm
Type of spontaneous abortion are defined by whether any or all of products of conception are
passed and whether or not the cervix is open. Differentiation of different types of spontaneous
abortion is thus contingent on history of the bleeding, any associated features such as
cramping and passage of tissue (including nature of passed tissue), examination of the cervix
to assess for dilation, as well as ultrasound to determine whether the fetus is still viable and
whether there remain any products of conception.
• Complete abortion: complete expulsion all POC <20 weeks
• Incomplete abortion: partial expulsion some but not all POC <20 weeks
• Inevitable abortion: no expulsion of products, but PV bleeding and dilation such that
viable pregnancy unlikely
• Threatened abortion: any PV bleeding <20 weeks, without dilation of cervix or
expulsion of POC (i.e. normal pregnancy with bleeding)
• Missed abortion: death of embryo or fetus <20 weeks with complete retention of
Bleeding +/- cramps
Bleeding + cramps +/- ROM
Heavy bleeding + cramps,
soft abdo, may have passage
of tissue
Bleeding + complete sac and
placenta passed
Fetal death and retention of
products, presenting as nonprogressing pregnancy
3 or more consecutive
spontaneous abortions
Closed – intact
Open >2cm
Watch and wait
<5% proceed to abort
D&C +/- oxytocin
D&C +/- oxytocin
No D&C
D&C +/- oxytocin
For genetic, medical and
psych reasons
Contents of uterus infected
before, during or after
• Mechanical: uterine
anatomy, cervical
• Autoimmune: lupus,
• Karyotype: both parents
• Endo: hypothyroid, DM
• Maternal infection
• Environment: smoking,
alcohol, drugs, radiation
D&C, IV broad spectrum
ABx, O2
Early pregnancy loss (major causes, steps in management)
Cameron Korb-Wells & Kai Brown (2009)
In management of bleeding in early pregnancy:
o ALWAYS rule out an ectopic
o ALWAYS check Rh status before D&C
o ALWAYS ensure patient is haemodynamically stable
Causes 1 /3 loss
o Chromosomal abnormalities: 60-80% spontaneous abortions in 1
trimester, potentially higher as also occur before implantation
o Other factors: infections, maternal anatomic defects, immunologic factors,
endocrine factors
o Large number have no obvious cause
o Stabilise all pregnant and bleeding patients if hypotensive
o Anti-D for all Rh-negative women with vaginal bleeding during pregnancy
o Complete abortion: follow for recurrent bleeding and signs of infection
(temp), send any tissue passed to pathology  assess POC have passed
and chromosome analysis if applicable
o Incomplete/ missed/ inevitable abortions: allow to finish if patient prefers
expectant, though may also complete with D&C or prostaglandins
(misoprostol) to induce dilation and uterine contractions
o Threatened abortion: follow for continued bleeding, pelvic rest with nothing
PV. Often bleeding will resolve, though at increased risk for PPROM and preterm labour
* Administer anti-D to all Rh negative mothers
Mid-trimester pregnancy loss (possible causes, discuss their management)
Causes 2 /3 loss: often multiple aetiologies
o Infection
o Anatomic defects: maternal uterine or cervical
o Maternal systemic disease
o Fetotoxic agents
o Trauma
o Stabilise all pregnant and bleeding patients if hypotensive
o Anti-D for all Rh-negative women with vaginal bleeding during pregnancy
o Incomplete/ missed abortions: allow to finish though often completed with
D&E. fetus larger in 2 /3 making procedure more difficult. From 16-24
weeks, D&E may be performed or labor induced with high dose oxytocin or
 D&E: self-limited and faster than induction of labor, though
aggressive dilation is necessary prior to procedure with laminaria
 Induction of labor: longer but allows completion without risks of
o Inevitable/ threatened abortions: important to rule out pre-term labor and
incompetent cervix, as uterine inability to maintain the pregnancy is likely
 Pre-term labor: begins with contractions leading to cervical dilatation
 tocolysis
 Incompetent cervix: painless dilatation  emergent cerclage
Cervical incompetence
• Background: painless dilation and effacement, often 2 /3. Dilation exposes fetal
membranes to vaginal flora and risk of trauma  infection, vaginal discharge and
ROM are common findings with incompetent cervix. May also have short-term
cramping or contracting and advancing cervical dilation.
• Epi: ~15% all 2 /3 losses
• Risk factors: often none known
o Cervical surgery (cone biopsy, D&C)
Cameron Korb-Wells & Kai Brown (2009)
Cervical lacerations with vaginal delivery
Uterine anomalies
DES exposure history
Hx: dilated cervix on routine exam, U/S or with bleeding/ discharge/ ROM.
Occasionally mild cramping or pressure in lower abdo/ vagina.
O/E: dilated more than expected with level of contractions (often difficult to
differentiate incompetent cervix and pre-term labor)
Viable  betamethasone, expectant management with bed rest and
tocolysis if contractions
Pre-viable (<24 weeks)  cervical cerclage, suture placed vaginally around
cervix. Complications include ROM, pre-term labor, infection. Usually offer
elective cerclage with subsequent pregnancies 12-14 weeks and removed
36-38 weeks. Transabdominal cerclage may be offered if transvaginal fails,
and deliver via C/S.
Examine pregnant patient bleeding in 1 trimester and make diagnosis
Differential diagnosis of first and second trimester bleeding
• Physiological bleeding: spotting, due to implantation of placenta  reassure and
check serial b-hCG
• Abortion (threatened, inevitable, incomplete, complete)
• Abnormal pregnancy (ectopic, molar)
• Trauma (post-coital)
• Genital lesion (e.g. cervical polyp, neoplasms)
History from a patient with previous miscarriage and discuss likely causes
Aetiology of miscarriage and recurrent miscarriage is as above outlined for spontaneous
abortions. Patients who suffer recurrent mischarriages should be evaluated for aetiology.
• Mechanical: uterine anatomy, cervical incompetence
• Autoimmune: lupus anticoagulant, antiphospholipid antibody (15% of recurrent loss)
• Karyotype: both parents
• Endocrine: hypothyroid, DM, luteal phase defect (inadequate progesterone)
• Maternal infection
• Environment: smoking, alcohol, drugs, radiation
o Karyotope of both parents, as well as products of conception from each
pregnancy if available
o Maternal anatomy should be examined, with hysterosalpingogram +/hysteroscopic or laporoscopic exploration
o Screening tests for hypothyroidism, DM, antiphospholipid antibody
syndrome, hypercoaguability and SLE
 Lupus anticoagulant, factor V Leiden, prothrombin G20210A
mutation, ANA, anticardiolipin, Russell viper venom, antithrombin III,
protein S, protein C
o Serum progesterone level in luteal phase
o Cultures of cervix, vagina and endometrium to rule out infection
o Endometrial biopsy during luteal phase to look for proliferative endometrium
o Chromosomal: IVF, PGD
o Anatomic: +/- correction of underlying abnormality
o Luteal phase defect: progesterone supplementation
o Antiphospholipid antibody syndrome: low-dose aspirin
o Thrombophilia: subcutaneous heparin (LMW or UF)
o Maternal diseases: appropriate Rx
Cameron Korb-Wells & Kai Brown (2009)
Lower abdominal pain (differentiating signs and symptoms)
Termination of pregnancy (ethical and medicolegal issues)
Medicolegal aspects
• NSW Crimes Act 1900 says that unlawfully procuring an abortion is an offence
punishable by imprisonment for up to ten years, and unlawfully supplying "any drug or
noxious thing, or any instrument or thing whatsoever" for the purpose of procuring an
abortion is punishable by imprisonment for up to five years.
• Levine Judgement: lawful and unlawful abortion: circumstances in which abortion
lawful expanded in 1971 by NSW District Court
o Abortion lawful if the doctor believes on reasonable grounds that it is
necessary to avoid a serious danger to her life or her physical or mental
health, taking into account economic and social factors as well as
medical ones, and the risks of the abortion are not out of proportion to the
danger to be averted. Women are not entitled to abortion on demand
• Availability: usually done between 7-12 weeks from first day of LMP. In NSW,
abortion available up to 18-20 weeks. Must be carried out by registered doctor
through clinics and public or private hospitals. Women in NSW do not need a referral
from a doctor to a clinic, which means a woman can call direct to the clinic for an
• Informed Consent: information about the procedure, possible risks and
complications, information on psychological and emotional feelings commonly
experienced after the abortion
• Women under 16 years: woman 14 and 15 years of age may give valid consent to
an abortion without her parent or guardian's knowledge. That is, if the doctor judges
the young woman to be mature enough to understand the implications of making the
• Women under 14 years: under 14 years of age should have the consent of a parent
or guardian or an order from the Supreme Court before a doctor would perform an
• Women with an intellectual disability: over 14 years of age has same rights if able
to give informed consent. If over 16 and lacks ability to give informed consent then
the Guardianship Tribunal can give consent on her behalf.
• Parenting rights: arise at birth, so only the woman (if able to make an informed
consent) and doctor have the right to decide on whether the best option at the time is
to have an abortion.
Approach to management
• Medical management
o < 9 weeks use methotrexate plus misoprostol
o > 12 weeks use prostaglandins intra- or extra-amniotically, or IM
• Surgical management
o < 12-16 weeks use dilatation and curettage
o > 16 weeks use dilatation and evacuation
• Complications
o Pain, bleeding, low-grade fever
o Perforation of uterus
o Haemorrhage
o Laceration of cervix
o Risk of sterility
o Infection/ endometritis - usually due to retained products
o Asherman syndrome (fibrosis of the uterus)
Trophoblastic disease (Dx and Rx)
Background: spectrum of proliferative abnormalities of trophoblast, 1/1000
pregnancies, cure >90%. 80% benign, 15% locally invasive, 5% metastatic
Complete mole: most common, diffuse trophoblastic hyperplasia, hydropic swelling
of chorionic villi, no fetal tissues or membranes
Cameron Korb-Wells & Kai Brown (2009)
Aetiology: 2 sperm fertilise empty egg or 1 sperm with reduplication  46XX
or 46XY paternal origin
o Risk factors: maternal age >40, diets low in beta-carotene, vit A deficiency
o Clinical features: b-hCG >100,000, vaginal bleeding (97%), excessive
uterine size (51%), theca-lutein cysts >6cm (50%), pre-eclampsia (27%),
hypremesis gravidarum (26%), hyperthyroidism (7%), no fetal heart detected
o High malignant potential: 4% after Rx, haematogenous to lungs (80%),
vagina (30%), pelvis (20%), liver (10%), brain (10%)
Partial mole: hydropic villi and focal trophoblastic hyperplasia associated with fetus
or fetal parts
o Aetiology: single ovum fertilised by two sperm  often triploid
 Usually associated with fetus that is growth-restricted with multiple
congenital abnormalities
o Clinical features: no dramatic clinical features, similar to threatened/
spontaneous/ missed abortion and pathologic diagnosis after D&C
o Low malignant potential
Ix: diagnosis based on ultrasound and b-hCG levels, with follow-up of these levels
important in identifying progression
o U/S: complete  no fetus and “snow storm” due to swollen villi; partial 
molar degeneration of placenta with developing fetal parts, multiple
echogenic regions of hydropic villi and focal haemorrhage
o b-hCG: abnormally high
o At-risk features for persistence: local uterine invasion >30%, b-hCG
>100,000, excessive uterine size, prominent theca-lutein cysts
Rx: D&C with sharp curettage and oxytocin, anti-D if Rh negative, +/- hysterectomy (if
patient doesn’t want further fertility) … +/- prophylactic chemotherapy or for those
persisting post-evacuation
F/U: contraception to avoid pregnancy in follow-up period, serial b-hCGs until
negative x3 (usually 3-10 weeks), then monthly for 6 months. If plateaus or increases,
patient needs chemotherapy
Malignant trophoblastic neoplasia
o Invasive mole or persistent hydatidiform mole: rising or plateau in b-hCG,
develop of mets following treatment  histology shows molar tissue,
metastases are rare.
o Choriocarcinoma: often presents with metastases, highly anaplastic and
vascular, may follow molar pregnancy, abortion, ectopic or normal pregnancy
o Placental-site trophoblastic tumour: rare aggressive form of
choriocarcinoma with abnormal growth of intermediate trophoblastic cells 
low b-hCG, production of hPL, insensitive to chemo
o Ix:
 Bloods: FBC, UEC, b-hCG, TSH, LFT
 Imaging: CXR, U/S pelvis, CT abdo/pelvis, CT brain
 Further: if suspect brain mets but CT (-)  LP for CSF hCG
o Rx: chemo (MTX)
o Prognosis: good or bad (bad = long duration >4/12, high b-hCG titer,
brain/liver mets, significant prior chemo, following term pregnancy)
o F/U: contraception, weekly b-HCG until 3 consecutive normal results then
monthly for 12 months or 24 months if to brain/liver/kidney/GI
Ectopic pregnancy (aetiology, pathology and Rx)
• Amenorrhea
• Abdominal pain (usually unilateral)
• Vaginal bleeding or spotting.
Background: implantation outside uterine cavity – tubes 99%, though also ovary,
cervix, abdominal wall, bowel
Cameron Korb-Wells & Kai Brown (2009)
Epidemology: 1/100 pregnancies, fourth leading cause of maternal mortality.
Incidence increasing  assisted fertility, STIs/ PID. Vaginal bleeding and/or abdo
pain should always be evaluated for ectopic.
Risk factors: 50% due to damage of fallopian tubes from PID
o Demographics: older women
o Smoking
o Endometriosis
o Gynaecologic: IUD, PID (esp C trachomatis), infertility, clomiphene
o Previous procedures: any tubal surgery (ectopic, tubal ligation), abdo
surgery for ruptured appendix, IVF pregnancies following ovulation induction
(7% ectopic rate)
o Structural: uterine leiomyomas, adhesions, abnormal uterine anatomy (Tshaped uterus)
o Prior ectopic: recurrent risk
Dx: history, physical examination, lab tests, ultrasound
o History: unilateral pelvic/ lower abdominal pain, PV bleeding
o Exam: temperature >38*C (20%), abdominal tenderness (90%), rebound
tenderness (50%), adnexal mass (50%), uterus small for gestational age,
bleeding from cervix
 Ruptured  hypotension, unresponsive, peritonitis (haemo)
o Lab: b-hCG low for gestational age and not increasing at expected rate
(doubling or at least 2/3 increase every 48 hours), Hct may be low with
o Ultrasound: may identify adnexal mass or extrauterine pregnancy. Only
definite if fetal cardiac activity detected in tube/ uterus. If yolk sac in uterus,
still risk of heterotopic pregnancy (i.e. multiple gestation with at least one IUP
and one ectopic)
 Rule-out ectopic: cannot definitively diagnose ectopic versus IUP  if
stable on exam, follow with serial b-hCG 48 hours.
Rx: be conservative and preserve tube if possible. 15% risk of persistent trophoblast
with surgical management – monitor b-hCG until undetectable.
o Ruptured: stabilise with IV fluids, blood products, pressors  laporoscopy to
stop bleeding and remove ectopic. Resection can be salpingostomy or
salpingectomy if tube damaged or ipsilateral recurrence. May require
o Unruptured: methotrexate 50mg/m single IM dose (~1/5 chemo dose) and
follow-up b-hCG until non-detectable. Success 67%, with ~25% requiring
additional dose. Tubal patency post-MTX ~80%.
 Criteria for medical management: clinically stable, <3.5cm unruptured
ectopic, no fetal heart activity, b-hCG<5000, no hepatic/renal/haem
disease, compliant and will follow-up
Prognosis: 9% maternal deaths, 40-60% pregnant again following surgery, 10-20%
subsequent ectopic.
Cameron Korb-Wells & Kai Brown (2009)
1. Define the puerperium and explain the anatomical and physiological
changes that occur in normal involution and lactation
Puerperium – 6 weeks after delivery
 Uterus involutes (1kg to 100g)
o Uterine vessels undergo hyaline changes
 Afterpains (esp. whilst suckling)
 Cervix becomes firm over 3 days
o Internal os closes day3, external os week 3
 Lochia (endometrial slogh) is passed
o Red for first 3 days
o Yellow then white over next 10 days until week 6
 Sudden drop in oestrogen > Breasts produce milky D/C (colostrum to day 3),
swollen and red with engorgement at day 3-4.
 Marked leukocytosis and thrombocytosis (with lymphopenia and
eosinophilia), Hb fluctuates. Haematology normal by 2 weeks.
2. Identify by history and examination the normal progress of the mother
and baby in the puerperium and discuss the effect of the baby on the
family unit.
3. Discuss the emotional changes and needs in the normal puerperium,
describe the symptomatology and management of puerperal psychosis
and recognise the effects of an abnormal puerperium on the family,
particularly in the areas of baby separation and grieving
4. Assist in the care and feeding of the normal baby and identify breast
problems in the puerperium and their management.
5. Examine a baby in the nursery to detect clinically obvious congenital
abnormalities and other neonatal abnormalities
6. Discuss appropriate advice on sexual relations and family planning on
the normal puerperal mother.
 Psychosocial
o Bonding
o Cheap
o Hygenic
o Convenient
 Protection against infection – Humoral + cellular
o IgA
o Complement + lysozyme + lactoferrin
o lymphocytes
o Less GI infections, pneumonia, OM
 Allergy
o Incidence of protein intolerance much less
o ↓ GI, resp and skin allergies
Cameron Korb-Wells & Kai Brown (2009)
o ↓ IBD,
o Ideal for digestion/absorption, micronutrients, fat:protein:carbs ↓ risk
juvenile DM-II
o Bottle fed babies are bigger and ? ↑ risk of obesity
 Breast engorgement ± mastitis ± abscesses
 Father less able to feed / bond / give mum a break
 Breastfeeding CI in HIV, amiodarone, antimetabolites, antithyroid drugs, opiates.
Newborn Baby Check
Usually done at 24-48 hrs (for PDA to close, and clinically relevant murmurs to become
• Obstetric (grav/pari, maternal complications, gestation)
• Antenatal (incl. serology, GBS, scans)
• Perinatal (delivery mode, complications, nursery admission, feeding)
• General medical history from mother.
• Observe for any jaundice, morphological deformities, any respiratory distress.
• Start head  toe
• Check fontanelles + suture lines
• Listen to heart sounds, HR, breath sounds, air entry, RR.
• Feel abdomen for masses, feel for femoral pulses
• Look for talipes equinovarus.
• Check 5x fingers, 5x toes.
• Place fingers in palm to check for grasp reflex
• Lift baby slightly to check for neck tone
• Lift to do stepping reflex
Turn over
Check for spinous processes, dimpling, tufts of hair, midline moles, Mongolian spot.
Lay prone and assess for limb tone/movements
Lay supine
Test flor Moro’s reflex
Test for sucking reflex
Test equal leg length
Do Barlow’s (for lig. laxity) and Ortalani’s (for hip relocation) manoeuvres.
 lactational amenorrhoea
o Prolactin suppresses gonadotrophin surges
o 98% effective in mothers who are solely breastfeeding and <6mo postpartum (↓ with less freq. no night feeding etc.)
o Mothers still menstruate
 Progesterone only pill
o Can start immediately or after day 21 (but barrier protection needed for
day 22 and 23)
o Low secretion in milk, no effect
o Can also get progesterone implants.
 Combined pills
Cameron Korb-Wells & Kai Brown (2009)
Oestrogen stops milk production (although can be used from 6wks, with
o Start at 3 weeks prost partum.
Intrauterine Contraceptive Devices
o Insert within first 48hrs or if not, after 4 weeks. (to minimise risk of
perforation upon insertion)
Barrier protaction
Sterilisation e.g. at caesarean section.
7. Describe and identify the abnormal puerperium including the clinical features of:
(a) abnormal bleeding
(b) infection
(c) thrombosis and embolism
(d) disturbances of bowel and bladder function
The 8 Bs: Blues (post-partum), Breathing (DVT/PE), Breast, Belly, Bowels, Bladder, Bleeding,
Puerperal Pyrexia
 temp over 38 in first 2 weeks.
o Examine lungs, breast, lochia, bimanual vaginal examination.
o 90% are GU infection
 Culture MSU, high vaginal swabs, blood and sputum
 Endometritis
o Offensive lochia, lower abdo pain, tender uterus
Post partum fever/bleeding – consider retained placenta (requires US + exploration and
Can have persistent urinary stress incontinence / bowel incontinence post partum.
8. Advise the mother how to obtain information regarding:
(a) Birth Registration Forms
(b) Available Health Services
(c) Maternity Allowances
(d) Available Social Services
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to understand the physiology of
conception and the factors which can prevent pregnancy so that you can initiate management
of patients with infertility and advise patients about contraception.
Structure and function of human reproductive organs
 External genitalia: collectively vulva
o Blood supply  internal pudendal artery
o Sensory innervation  pudendal nerve
o Lymphatic drainage  inguinal nodes
Vagina: muscular canal from cervix to vulva, anterior to rectum and posterior to
bladder  lined by rugated stratified squamous epithelium, upper vagina separated
by cervix to anterior/ posterior/ lateral fornices
o Blood supply  vaginal branch internal pudendal with anastomoses from
uterine/ inferior vesical and middle rectal arteries
Uterus: thick walled muscular organ between bladder and rectum, consisting of
uterine corpus and cervix
o Blood supply  corpus = uterine artery (branch of internal ilac), cervix =
cervical branch of uterine artery
o Position  anteverted (majority), retroverted
o Supported by pelvic diaphragm and pelvic organs and 4 paired sets of
 Round ligaments  anterior uterus, through broad ligaments,
through inguinal canals, terminate in labia majora  keeps uterus
 Uterosacral ligaments  arise sacral fascia and insert posterior
inferior uterus  mechanical support for uterus and contain
autonomic nerve fibres
 Cardinal ligaments  from lateral pelvic walls inserting into lateral
cervix and vagina  mechanical support, preventing prolapse
 Broad ligaments  from lateral pelvic wall to sides of uterus 
coursing through broad ligament on each side is fallopian tube, round
ligament, ovarian ligament, nerves, vessels and lymphatics
Cameron Korb-Wells & Kai Brown (2009)
Physiology of menstrual cycle
Actions of female sex hormones
Cameron Korb-Wells & Kai Brown (2009)
Factors necessary for fertilisation and implantation
 Ovary
 Tube
 Cervix
 Endometrium
 Male
Contraception and relative efficacy
Contraception should be available to all women and men of reproductive ages. Education
about contraception and access to contraceptive pills or devices are especially important for
sexually active teenagers and for women following childbirth or abortion.
In weighing risks and benefits of contraception benefits, couples must keep in mind that no
contraceptive or sterilisation method is 100% effective.
• Theoretical efficacy rate: efficacy when used exactly as instructed
• Actual efficacy rate: efficacy when used in real life, assuming variations in
consistency of usage
• Withdrawal/coitus interruptus
• Periodic abstinence
• Lactational amenorrhea
• Chance (no method used)
• Complete abstinence
• Condom alone
• Condom with spermicide
• Spermicide alone
• Sponge
• Diaphragm with spermicide
• Female condom
• Cervical cap: parous
• Cervical cap: nulliparous
• Nuvaring
• Skin patch
• Depo-provera
• Implanon
• Progestin-only pill
• Mirena
• Copper
• Tubal ligation
• Vasectomy
Cameron Korb-Wells & Kai Brown (2009)
98% (1 6 months postpartum)
98-99.5% (depending on compliance)
Emergency postcoital
• Yuzpe method
• ‘Plan B’ levonorgestrel only
• Postcoidal IUD
98% (within 24 hours)
98% (within 24 hours)
Natural methods: physiology-based methods using neither chemical nor mechanical means
 pursued largely with religious/ philosophical reasons. LEAST effective and shouldn’t be
used if contraception is high priority
• Periodic abstinence: fertility awareness and abstinance shortly before and after
estimated ovulation  ovulation prediction kits, basal body temperature
measurements, menstrual cycle tracking, cervical mucous evaluation, documentation
of premenstrual/ ovulatory symptoms
o Efficacy: 55-80% (very low cf others)
o Adv/dis: natural, requires significant motivation, requires regular prolonged
periods of abstinance and regular cycles
• Coitus interruptus: withdrawal before ejaculation, with majority of semen deposited
outside female reproductive tract
o Efficacy: ~73% (pre-ejaculate, near introitus)
o Adv/dis: high failure rate, self-control
• Lactational amenorrhoea: after delivery, restoration of ovulation delayed from
hypothalamic suppression of ovulation from prolactin-induced inhibition of pulsatile
o Efficacy: 45-85% (50% lactating mothers ovulate within 6-12 months, note
ovulation occurs prior to first period)  use for MAX 6 months post-delivery
 Adv/dis: cheap, though unreliable
Barrier methods: prevent sperm entering endometrial cavity and tubes
• Male condoms
• Female condoms
• Diaphragm
• Cervical cap
• Spermicides
Mirena: progesterone-releasing, works by decidualising endometrium and thickening
cervical mucous, may suppress ovulation
Copper: mild foreign body reaction in endometrium toxic to sperm and altering sperm
Efficacy: 95-99% (failure rate 0-1.2%)
Duration: 5 years
Adv: reversible, private, convenient, may be used in women with C/I to OCP or
wanting long-term contraception
Dis (risks): expulsion higher in young/ low parity women, ectopic pregnancy, septic
abortion, uterine perforation (time of insertion), PID
Absolute C/I: known/ suspected pregnancy, undiagnosed genital tract bleeding, acute
or chronic PID, lifestyle risk for STIs, known allergy to copper, Wilson’s disease (latter
2 copper IUD only)
Relative C/I: nulliparity, valvular heart disease, past history PID/ ectopic, presence of
prosthesis, abnormalities of uterine cavity (intracavitary fibroids), severe
dysmenorrhoea or menorrhagia (copper), cervical stenosis, immunosuppressed
• Combined oestrogen and progestin OCP: most contain low dose ethinyl oestradiol
(20-35ug) plus progestin (norethinedrone, levonorgestrel, desogestrel, norgestimate,
drospirenone)  monophasic or triphasic formulations (varying oestrogen/progestin
exposure through cycle)
o Efficacy: 98.0-99.5% (depending on compliance)
Cameron Korb-Wells & Kai Brown (2009)
Mechanism of action: ovulatory suppression by inhibiting LH and FSH, also
decidualisation of endometrium and thickening of cervical mucous to
decrease sperm penetration
Advantages: highly effective, reversible, regulates cycles, decreases
dysmenorrhoea and menorrhagia, less benign breast disease/ ovarian cyst
development, lower ovarian/ endometrial cancer risk, increases cervical
mucous (? Lower risk STIs), decreases PMS, improves acne, protects
against osteoporosis
Side effects
 Oestrogen-related: nausea, breast (tenderness, enlargement), fluid
retention/ bloating/ oedema, weight gain, migraines/ headaches,
thromboembolic events/ liver adenoma (rare), intermenstrual
bleeding (low oestradiol)
 Progestin-related: amenorrhea/ intermenstrual bleeding, headaches,
breast tenderness, increased appetite, decreased libido, mood
changes, hypertension, acne/ oily skin*, hirsuitism* (* androgenic s/e
minimised by pill with desogestrel/ norgestimate)
 Interactions decreasing efficacy (requiring backup): rifampin,
phenobarbital, phenytoin, primidone, VOMITING/DIARRHOEA, St
John’s wort
 Conception despite OCP: no evidence fetal anomalies
 Breastfeeding: no evidence harmful but may decrease milk
production, so wait 6 weeks postpartum
 Reduced cancer risk: ovarian risk reduced 50%, colorectal reduced
18-40%, endometrial reduced 50%
 Increased cancer risk: cervical cancer risk slightly increased, as is
breast though literature conflicting
• Counselling: eg, if 10 women per 1000 are expected to have
a diagnosis of breast cancer by age 45, use of the COCP
can be attributed to add one more case per 1000
• WHO recommendations in specific conditions:
o Benign breast disease or family history of breast
cancer in first-degree relative under 45 (WHO 1) –
o Previous breast biopsy with epithelial atypia (WHO
4) – don’t use
o Breast cancer diagnosed less than five years ago
(WHO 4) – don’t use
o Women developing breast cancer while using the
COCP (WHO 4) – don’t use
o Known inherited breast cancer gene mutation (WHO
3) – usually
Absolute C/I
 O&G: known/ suspected pregnancy, undiagnosed abnormal vaginal
 Thromboembolic: smoker >35 years, prior thromboembolic events,
thromboembolic disorder (protein C/S/antithrombin III, Factor V
Leiden), active thrombophlebitis
 Neoplastic: oestrogen-dependent tumours
 Metabolic: CVD, CHD, congenital hypertriglyceridaemia, uncontrolled
 Other: migraines with focal neuro symptoms (excluding aura),
impaired LFTs
Relative C/I: migraines (nonfocal with aura <1 hour), DM with vascular
disease, SLE, controlled hypertension, hyperlipidaemia, sickle cell anaemia,
gallbladder disease
Starting OCP: thorough Hx and exam (including breast), start first week of
active tablets on day 1-5 of menses for immediate effect, follow-up in 6
Cameron Korb-Wells & Kai Brown (2009)
weeks after OCP prescribed, pelvic exam may be delayed until subsequent
Missing pills/ vomiting/ diarrhoea
 Forget to take inactive pill: contraception not affected
 Vomit within 2 hours of active pill: take another active pill as soon as
 <24 hours late taking active pill: take as soon as remember and take
next pill at usual time; contraception will not be affected.
 >24 hours late taking active pill, or severe vomiting or diarrhoea
>24 hours: pill will not be as effective in preventing pregnancy:
• if late taking active pill take as soon as remember and next
pill at usual time
• continue with the daily pill but use another contraceptive
method (eg condoms) or avoid intercourse until active pills
for 7 days
• if 7 days extend into inactive pill/pill-free week, do not break
from active pills; finish active pills in present pack then
proceed directly to active pills in new pack (period will be
delayed until end of new pack, though may spot or bleed
especially taking triphasic pill)
 Emergency contraception if missed pill in 7 days after inactive pill/pillfree week and had intercourse during or after that time
Changing preparations
 Changing a higher or same dose pill, take as normal including
inactive pills
 Changing to a lower dose pill, miss any inactive pills and start taking
the new pill without an inactive pill/pill-free interval.
 Changing from progestogen-only pill to combined pill, start taking
active pill without any interval.
Types: OCP containing gestodene, desogestrel, dienogest, drospirenone and
cyproterone not listed on PBS and may be significantly more expensive for
 Levonorgestrel, norethisterone (LEVLEN, MICROGYNON,
BREVINOR): lower risk of VTE than others
 Gestodene, desogestrel (MARVELON, MINULET): less
androgenic activity than levonorgestrel, however, almost twice risk of
VTE compared to levonorgestrel or norethisterone. Generally not
first choice for new users but may be used for those not tolerating
other progestogens, provided the woman is given estimates of VTE
 Dienogest (VALETTE): anti-androgenic activity (approximately onethird of cyproterone). Beneficial effects on acne but unclear whether
advantages over others. Limited data regarding VTE risk.
 Drospirenone (YASMIN/YAS): Related to spironolactone, antimineralocorticoid (mild diuretic and potassium retention) and antiandrogenic activity. Incidence of VTE similar to levonorgestrel.
Unclear whether drospirenone can cause hyperkalaemia if used in
women with renal impairment or taking drugs which increase
potassium concentration. It is available in 2 different regimens.
• Yasmin : similar effects on skin, contraceptive efficacy and
cycle control as gestodene or desogestrel; compelling
evidence lacking for any particular benefit for Yasmin ,
eg less weight gain or reduced androgenic effects.
• Yaz : low dose ethinyloestradiol in regimen with active
tablets 24 days in 28-day cycle. Shortening hormone-free
interval thought to reduce incidence of hormone withdrawal
symptoms and may increase effectiveness by further
suppressing ovarian function. Compared to placebo, Yaz
beneficial effects on acne and may help treat symptoms of
PMS but no direct comparisons to other pills.
Cameron Korb-Wells & Kai Brown (2009)
Cyproterone (DIANE, ESTELLE, JULIET): Progestogenic and antiandrogenic. Used with oestrogen to treat women with
androgenisation (eg severe acne, idiopathic hirsutism); combination
also provides effective contraception. This combination is associated
with higher incidence of VTE compared to others and is not indicated
in absence of androgenisation.
Hormonal contraceptive skin patch: continuous release 6mg norelgestromin +
0.6mg ethinyl oestradiol into bloodstream, through patch applied to lower abdomen/
back/ upper arm/ buttocks. Patch worn weekly for 3 consecutive weeks (changing
weekly) with 1 week off to allow menstruation
o Efficacy: as effective as OCP (>99% with perfect use, though 3% failure with
regular use), may be less effective in women >90kg
Hormonal contraceptive ring (Nuvaring): thin flexible plastic ring inserted high
vaginally, releasing etonogestrel 120ug/d + oestradiol 15ug/d, working for 3 weeks,
then remoed for 1 week to allow menstruation
o Efficacy: as effective as OCP (98%), avoids first pass effect
o S/E: vaginal infection/ irritation, vaginal discharge
Progestin only: postpartum women, contraindication to combined OCP
(thromboembolic/ myocardial disease) or those intolerant of oestrogen S/E
o Mechanism: thickening of cervical mucous, decreased tubal motility,
endometrial suppression, ovulation suppression
o S/E: irregular menstrual bleeding, weight gain, headache, breast tenderness,
mood changes, functional ovarian cysts
o Minipill (norethisterone - Micronor): taken daily at same time of day (within 3
hours) to ensure reliable effect, no pill free interval, higher failure rate than
other hormonal methods (1.1-13%, 0.51% perfect use). Ovulation inhibited
60% of women, most have regular cycles.
o Depo-provera: injectable depot medroxyprogesterone acetate 150mg IM q1214 weeks. Convenient. Initiate within 5 days of normal menses or
immediately postpartum. Irregular spotting progresses to complete
amenorrhoea in 70% of women (1-2 years of use). Highly effective 99%,
failure rate 0.3%. Side effects of decreased bone density with only partial
recovery, with restoration of fertility taking up to 2 years.
 Recommend: Ca, vit D, weight-bearing exercise, smoking cessation,
decreased alcohol, reduced caffeine
o Implanon: single-rod progestin implant that releases the progestin
etonogestrel (40 mg/day); it provides contraception for up to 3 years. 2-year
multicenter study of 330 sexually active women found Implanon to be a safe,
highly effective, and rapidly reversible means of contraception (>99%)
Emergency contraception
• Emergency contraceptive pills (hormonal)
o Mechanism: suppress ovulation or cause deficient luteal phase, may alter
endometrium to prevent implantation, may affect sperm/ova transport
o S/E: nausea (oestrogen, treat with dimenhydrinate), irregular spotting
o C/I: pre-existing pregnancy (though not teratogenic), caution in women with
C/I to OCP (though no absolute C/I)
o Yuzpe method: any OCP with 100ug ethinyl oestradiol PO q12h x 2 doses
used within 72 hours, limited evidence of benefit up to 5 days
 2% overall pregnancy risk (efficacy decreases with time)
o “Plan B”: levonorgestrel 750ug q12h x2 doses within 72 hours and better S/E
profile then Yuzpe method (no oestrogen therefore little C/I)
 Efficacy 75-95% if within 24 hours (decreasing with time)
• Emergency IUD insertion
o Postcoital Copper IUD: insert up to 7 days postcoitus, to prevent
implantation. 1% failure rate. C/I and precautions similar to IUD. Can use for
short durations in high risk individuals
o F/U: 3-4 weeks post-treatment to confirm efficacy (spontaneous menses or
pregnancy test), contraception counselling
Cameron Korb-Wells & Kai Brown (2009)
Notes on mifepristone/RU-486
• Progesterone antagonist, used in conjunction with misoprostol as abortifacient and
licensed in UK/ USA/ Europe as emergency contraceptive.
• Listed on World Health Organisation’s list of essential medicines, as provides
effective and relatively safe method of medical termination of pregnancy
• Significant debate regarding licensing in Australia as emergency abortifacient
• In NZ, Mifepristone was approved by the New Zealand Medicine and Medical Device
Safety Authority (MEDSAFE) on 30 August 2001 for four indications:
o Early medical termination of pregnancy
o Priming cervix before surgical termination
o Second trimester medical termination of pregnancy
o Induction of labour for fetal death in utero.
• In Australia, mifepristone has not been approved for general use by the TGA. Unless
and until this occurs, practitioners may apply for authorized prescriber status (section
19(5) of the Therapeutic Goods Act 1989) or on a case by case basis through the
Special Access Scheme (SAS). The drug is not available through pharmacies but on
a restricted basis to institutions licensed to carry out termination of pregnancy
• Not available for use as post-coital contraceptive and alternative emergency
contraception (e.g. IUD, Postinor, etc) should be considered.
Sterilisation and medico-legal aspects
Before performing sterilisation, careful counseling should be provided and informed consent
obtained. Patient should understand permanent and largely irreversible nature of procedure,
operative risks, chance of failure, and possible side effects. Sterilisation is ideal in stable
monogamous relationships where no additional children are desired. Also indicated in women
in whom pregnancy would be life threatening such as those with major cardiac issues.
Tubal ligation
o Method of Action: surgical occlusion both fallopian tubes to prevent ovum
and sperm uniting. When performed outside postpartum period done via
laparoscopic (laparoscopic tubal ligation [LTL]) or hysteroscopic (Essure,
Adiana) approach.
 Laparoscopically: bipolar cautery, banding, clipping with Filshie clips
and ligation sutures
 Hysteroscopic transcervical nonincisional approach (Essure): flexible
form-fitting microinserts are introduced into the interstitial (uterine)
portions of the fallopian tubes. Outer spring coil molds to shape of
fallopian tube to anchor the microinsert. Over about 12 weeks,
sterilization is accomplished as in-growth of tissue around the coils
result in tissue barrier occlusion in the fallopian tubes. Backup
method recommended for 3 months after the procedure until
hysterosalpingogram can confirm complete tubal occlusion
o Effectiveness: failure rate of 0.5% but varies by method, age, and surgeon's
experience. Highest success in postpartum sterilization and Essure tubal
o S/E: some women report pain and menstrual disturbances
o Advantage/Disadvantages: permanent effective contraception without
continual expense, effort, or motivation. The mortality rate of bilateral ligation
4 in 100,000 women. Major risks are those associated with surgery (infection,
hemorrhage, conversion to laparotomy, viscus injury, vascular damage, and
anesthesia complications). Very low risk of pregnancy, though when does
occur increased risk of ectopic
o Reversal: regret highest in women under age 30 when procedure performed.
Success of reversal varies from 41% to 84% depending on method used.
Success rate of reanastomosis highest when clips used since destroy smaller
segment of tube. IVF may be offered.
o Method of Action: permanent sterilization involving ligation of the vas
deferens (local anesthesia through small incision in upper outer aspect of
Cameron Korb-Wells & Kai Brown (2009)
each scrotum). Also no-scalpel vasectomy where both vas ligated through
single small midline incision that reduces already low rate of complication.
 Not immediately effective! Sperm can remain viable in proximal
collecting system, therefore use another form of contraception until
azoospermia confirmed by semen analysis, usually in 6 to 8 weeks.
Effectiveness: failure rate 0.15% --> safer, simpler, and more effective than
female sterilization. When pregnancies occur, many due to having
intercourse too soon after vasectomy rather than from recanalization of the
vas deferens.
S/E: complications rare usually slight bleeding, skin infection, and reactions
to the sutures or local anesthesia. Fifty percent form antisperm antibodies
after the procedure.
Advantages/Disadvantages: permanent, highly effective contraception with
few, if any, side effects. Generally safer and less expensive than tubal
ligation and can be performed as an outpatient under local anesthesia.
Success rate of vasal reanastomosis is 60% to 70%. Pregnancy rates after
vasectomy reversal range from 18% to 60%.
Counselling individual/ couple in contraceptive techniques
Details above
Obtain thorough O&G history from patient, to identify features of the patient’s history which
might favour a particular method, and similarly identify any relative or absolute
Perform a thorough consultation discussing with the patient each of the following aspects:
 Options available (consider current age, fertility status, desire for future pregnancy)
o Barrier
o Hormonal: OCP, progesterone only mini pill, Nuvaring, Mirena, Implanon,
o IUCD: copper, Mirena
o Surgical: tubal ligation, vasectomy
 Relative efficacy (discuss concepts of theoretical vs actual efficacy)
 Side effects (+/- favourable S/E for patient circumstances)
o OCP C/I: pregnancy, high thromboembolic risk, known CVD
 Interactions: diminish efficacy of contraceptive effect
o Medications: rifampin, phenobarbital, phenytoin, primidone, vomiting/
diarrhoea, St John’s wort
 Duration of contraceptive effect, return to fertility
 Discuss with partner
Reach decision regarding most appropriate form of contraception in the woman’s individual
circumstance. Note different agents within same class may be preferable with respect to side
effect profile, etc)
If commencing OCP, factors to consider:
• Ascertain low pregnancy risk,— one or more of the following
o no intercourse since last normal menstrual period
o correct use of other method
o within seven days of onset of menses
o within seven days of miscarriage or termination of pregnancy
o fully or nearly fully breastfeeding less than six months postpartum
o after emergency contraception
• Obtain negative urine pregnancy test
• Begin in active section of packet in the office
• Seven days added condom use mandatory
• Early follow-up for all with repeat pregnancy test
Cameron Korb-Wells & Kai Brown (2009)
Written and verbal information on the method supplied
Counselling woman with pregnancy following contraceptive failure
 US figures: ~90% women of childbearing age use some form of contraception,
though still 50% pregnancies in US are unintended  43% live births, 13%
miscarriages, 44% elective abortion
 Presenting options: proceeding with pregnancy, adoption, elective termination
Investigation of infertile couple
 Infertility definition: failure to conceive after one year of regular unprotected
o Primary infertility: no prior pregnancies
o Secondary infertility: previous conception
 Background: infertility in 10-15% of couples. Normally 75% of couples achieve
pregnancy within 6 months, 85% within 1 year, 90% within 2 years. Both male and
female need to be investigated. Once the cause of infertility is identified, therapy is
aimed at correcting reversible conditions or overcoming irreversible conditions.
o Infertility is a complex medical disorder that requires the evaluation and
treatment of a couple rather than an individual
 When to begin investigations: time is evidently a more critical issue in older
o <35 years: after 1 year trying to conceive
o 35-40: after >6 months
o >40 years: immediately
o Earlier if: history of PID, infertility in previous relationship, prior pelvic surgery,
chemo/radiotherapy in either partner, recurrent pregnancy loss, moderatesevere endometriosis
 Causes
o 45% female factors
o 35% male factors
o 20 % mixed factor
o 10% unknown
 Overview of infertility evaluation: history and examination of both patients, semen
analysis to exclude male factor infertility (quick and easy to do), invasive procedural
investigations if clinical evidence of ovulatory cycles OR further endocrine bloods if
clinical evidence of anovulatory cycles
Cameron Korb-Wells & Kai Brown (2009)
Female factor infertility
 Causes: ovulatory disorders (32%), fallopian tube abnormalities (incl pelvic
adhesions) (34%) and endometriosis (15%)… also uterine and cervical factors, luteal
phase defect, and genetic disorders
 Ovulatory disorders: disruption in hypothalamic-pituitary-gonadal axis  menstrual
disorders, impaired folliculogenesis, ovulation, endometrial maturation. Four types, of
which PCOS and advanced maternal age are most common:
o (1) hypogonadotrophic hypogonadal anovulation (hypothothalamic)
o (2) normogonadotropic normoestrogenic anovulation (PCOS)
o (3) hypergonadotropic hypoestrogenic anovulation (premature ovarian failure,
advanced maternal age)
o (4) hyperprolactinaemic anovulation
 Tubal factors: tubal disease and pelvic adhesions prevent transport of oocyte and
sperm through fallopian tube. Primary cause pelvic inflammatory disease
(gonorrhoea, Chlamydia). Other conditions affecting tubal transport include severe
endometriosis, prior ectopic pregnancy, previous surgery/ nongynaecologic infection
(appendicitis, diverticulitis)
 Endometriosis: see above. ~15% infertile women. Mechanism of infertility not
understood, can interfere with tubal mobility, cause tubal obstruction or result in tubal/
ovarian adhesions holding fallopian tube away from ovary or trapping released
oocyte. However, infertility also diagnosed in women with minimal endometriosis and
no adhesive disease  ? inflammatory mediators impairing ovulation/ fertilization/
 Uterine/ cervical: <10% female factor infertility
o Uterine  fibroids, polyps, intrauterine synechiae, congenital malformations
(bicornuate). Endometrial  hyperplasia, out-of-phase endometrium,
carcinoma. Risk factors include PID, multiple D&Cs.
o Cervical  structural abnormalities, cervicitis, abnormal cervical mucous
production. Iatrogenic stenosis from cervical Rx.
 Luteal phase defect: controversial, ? inadequate progesterone from corpus luteum
with delay in endometrial maturation  impaired implantation
 Investigative approach
Cameron Korb-Wells & Kai Brown (2009)
Hx: full medical, surgical and menstrual  symptoms of menstrual
irregularity, hursuitism, thyroid dysfunction (PCOS), cyclic pelvic pain,
dysmenorrhoea, dyspareunia (endometriosis), STI
o Exam: signs of PCOS, thyroid dysfunction, pelvic exam (cervical stenosis,
fixed retroverted uterus in endometriosis)
o Ix:
 Evidence of ovulation: basal body temperature, cervical mucous,
mid-luteal progesterone
 Pap smear/ cervical cultures: for gonorrhoea and Chlamydia in all
 Endocrine evaluation: FSH, LH, prolactin, TFTs, thyroid antibodies,
? Cushing syndrome (testosterone, DHEAS, 17OH-progesterone, 24hour urine cortisol, overnight dexamethasone suppression test)
 Imaging: pelvic U/S (+/- saline sonohysterogram augmentation) 
uterus for structural defects; CT or MRI  where intracranial lesions
 Clomiphene citrate challenge test: 100mg days 5-9  FSH days 3
and 10, which rises if PCOS
 Progestin challenge test: for endometrial ability to bleed, progestin
5-10 days, withdrawal bleed within 1 week
 Procedural: laporoscopy  endometriosis or pelvic adhesions
suspected; hysterosalpingogram (follicular phase or tubal lavage)
during laporoscopy for anatomical abnormalities; hysteroscopy 
examine uterus
Treatment approach
o Identify and correct underlying aetiology: 90% of cases due to endocrine
abnormalities may be restored to fertility
 Uncorrectable: ovulation induction, intrauterine insemination or IVF
o PCOS: weight loss, metformin, clomiphene
o Hypothalamic-pituitary failure: pulsatile GnRH
o Premature ovarian failure: NO CURE, egg donation, adoption
o Endometriosis: laporoscopy for excision/ coagulation of periadnexal
adhesions and endometrial implants. Medical management may provide
symptomatic relief but no Rx improves fertility outcomes. Symptomatic
management may be achieved with danazol, leuprolide,
medroxyprogesterone or continuous OCP
o Tubal occlusion: tuboplasty with reanastomosis, though most undergo IVF
o Uterine factors: corrective operative hysteroscopy
o Cervical factors: varies with cause, surgical/ mechanical dilatation or cervical
byass with IUI
Male factor infertility
 Causes: multiple causes, including endocrine (Kleinfelters), anatomic defects,
abnormal sperm production/ mobility, sexual dysfunction
o Risk factors: occupational/ environmental exposure (chem., rad, excessive
heat), varicocoele, mumps, hernia repair, pituitary tumour, anabolic steroid
use, testicular injury, impotence, medication (cimetidine, sulfasalazine,
spironolactone, antidepressants, metoclopramide, chemotherapy, beta
blockers, nitrofurantoin)
 Investigative approach
o Hx: previous pregnancies, environmental exposures, meds, STIs, mumps
orchitis, hernia repair, surgery/ trauma
o Exam: signs of testosterone deficiency/ varicocoele, identify urethral meatus,
measure testicular size
o Ix:
 Semen analysis: sperm count, volume, motility, morphology, pH,
Normal semen analysis
>2 mL
Cameron Korb-Wells & Kai Brown (2009)
Concentration >20 million/mL
>30% normal forms
Motility >50% forward progression
<1 million/mL
 Endocrine (if semen abnormal): TFTs, testosterone, prolactin, FSH
 Postcoital test: interaction between sperm and cervical mucous
 Antisperm antibodies (if postcoital test abnormal)
Approach to treatment
o Improve coital practice: intercourse every other day near ovulation, avoid
tight underwear, saunas/ hot tubs and unnecessary radiation/ heat and
certain medications
o Identify and treat underlying aetiology: hypothalamic-pituitary failure with
injections of human menopausal gonadotropins, varicocoeles repaired by
o Assisted reproductive techniques: overcome abnormal semen analysis when
treatment of underlying disorder not effective
 Washed sperm for IUI with low semen volume/ sperm density/
 ICSI: for low sperm density/ impaired motility  obtained by
ejaculation or direct aspiration  prepared and injected into egg,
before intrauterine placement
 Donor sperm: refractory cases
Unexplained infertility
 When in-depth testing identifies no cause, most therapies have no higher success
rates than no treatment at all
o No treatment: 60% pregnancy over 3-5 years
o Donor sperm, surrogacy, adoption
Factors influencing human fertility (incl. psychological/ emotional sequelae)
Management of common causes of infertility
As above
Ethical implications of new reproductive technologies
Ethical issues of contraception including sterilisation
Cameron Korb-Wells & Kai Brown (2009)
1. Discuss the differences between pathological and physiological vaginal
2. Discuss the clinical circumstances that predispose to genital tract
3. List the likely organisms causing genital tract infection.
4. Discuss the sequelae of different types of genital tract infections.
5. Take and present a history from a patient with genital tract infection
and describe or demonstrate the expected physical signs.
6. Examine patient(s) and demonstrate an ability to differentiate
between normal vaginal secretion and pathological discharge.
7. Indicate the appropriate investigations that will aid the diagnosis and
management of genital tract infection.
8. Discuss the appropriate therapy for genital tract infections.
9. Explain the public health and the possible social implications of genital
tract infection with particular reference to viral conditions.
10. Understand of the implications and effects of AIDS on pregnant and
non-pregnant women and their infants.
11. Discuss the prevention of infections acquired via the genital tract
Vaginal Discharge
 White, curd-like, thick = thrush
 Grey-white, fishy = bacterial vaginosis
 Yellow, malodorous, itchy = Trichomonas vaginalis
 Thick, pus-like = Chlamydia or gonorrhoea
At Risk Groups
 Sex workers
 Younger persons
 Men who have sex with men (Syphilis, gonorrhea, HIV)
Organisms in Genital Tract Infection
 Parasites
o Scabies
 Spares face and scalp, worse at night
 Rx - permethrin cream, treat partner
o Public live
 Rx – as above
 Trichomonas vaginalis
o Protozoa, usually sexually aquired
o Low incidence in city, higher in rural
o Almost all men asymptomatic, 50% women asymptomatic
o Yellow, malodorous, itchy D/C
o Dx wet film, pap, PCR
o Rx – metronidazole + partner
 Candida Albicans
o Not considered an STI, but men can be secondarily infected
o Often recurrent, sometimes chronic
o Thick, white, curd-like D/C
o Dx wet film or swab
o Rx – oral/topical –azole
 Bacterial vaginosis
o Not an STI, although assoc. with sexual activity
o Assoc. with PID, PRM, miscarriage
o Pearly-grey, fishy smelling D/C
Cameron Korb-Wells & Kai Brown (2009)
 Pronounced after sex and pre-menstrually.
o Rx – metronidazole
Chlamydia Trachomatis
o Most common STI (10x > gonorrhoea)
o No Ab protection from prior infection
o Notifiable infection in NSW
o Most are asymptomatic
o Men – urethral D/C, dysuria, epididymitis
o Women – D/C, irregular bleeding, dyspareunia, PID, tubular damage, ↑ risk
ectopic preg/infertility in chronic infection.
o Can also get Reiter’s Arthritis and conjunctivitis.
o Dx – urine PCR, cervical/vaginal swab, thin prep. Serology useless.
o Rx – Azithromycin 1g stat + partner
 Doxycycline 200mg OD for 2/52 if PID
 If want to re-test for cure, do so at least 2/52 later.
Neisseria Gonorrhoea
o Symptoms may be absence or non-spec.
o D/C cannot be distinguished from chlamydial infection
o Woman may also get PID, Bartholian abscess.
o Can also get Reiter’s Arthritis and conjunctivitis.
o Notifiable infection in NSW
o Dx – swab D/C and send for culture (PCR available but cannot give
sensitivities – ciprofloxacin and penicillin resistant strains exist)
 May also swab cervix, anus, urethra, pharynx as per Hx.
o Rx – ceftriaxone 250mg IM stat + partner
 Consider treating for Chlamydia also (high co-infeciton rates)
o Commonest cause of genital ulcers
o Large number of serotypes (most common HSV2, although <20yrs HSV1)
o Primary infection lasts 14-21 days, subsequent attacks shorter.
o Dx – PCR for vesicle fluid
o Rx – acyclovir + symptomatic (saline, LA) education re: recurrance/shedding
Human Papiloma Virus
o Most common viral STI (79% of persons will have an episode, most clear
o 120 serotypes
o 16 oncogenic varieties
o Gardasil vaccine covers 6, 11 (90% genital warts) and 16, 18 (70% Ca)
 Greater immune response the younger the patient, max benefit if
given before first intercourse
o Time from inoculation to clinical exhibition may be years.
o Dx – PCR available but use limited as high background prevalence
o Rx – offer other STI screening, Pap smear (no more freq. than usual)
 Chemical – podophyllin (not in pregnancy)
 Physical – cryotherapy, electrocautery, surgical or laser
 Immune – imiquimod (better in woman than men, less recurrance)
• Rx of visible warts does not cure, most remain infectious
Treponema Pallidum (Syphilis)
o Painless ulcer or morbilliform rash (secondary)
o Dx – VRDL / RPR
o Rx – penicillin
Hepatitis A
o Can be spread via anal sex
Hepatitis B
o Trx via infected blood or secretions
o 3 dose vaccine available
Hepatitis C
o Mostly blood-borne rather than sexual
o High risk of chronic hepatitis than Hep B
Cameron Korb-Wells & Kai Brown (2009)
 To baby – 1:50 to 1:2
 Receptive anal sex – 1:125 to 1:31
 Contaminated IVDU – 1:149
 Insertive vaginal/anal – 1:333 to 1:111
 Needlestick – 1:313
 Receptive vaginal – 1:2000 to 1:667
Pre-test counseling
 Dx – ELISA then confirm on western blot
Rx – multiple regimes, principal is that must have multiple ARVD to minimize
risk of resistance
 ARVD + elective LSCS reduces vertical transmission to <2% (versus
20-30% not Rx)
NB: Bacterial vaginosis, Chlamydia and gonorrhea – PID, infertility, ectopic pregnancy
NB: Chlamydia, gonnorhoea, HIV, syphilis, Hep C – all notifiable
“STI and non-ST infections of the GU tract are very common in the community. Many patients
may be asymptomatic and some diseases are notifiable. My approach to treatment would be
to consider epidemiological aspects in considering screening at risk groups, definitive
treatment of the patient and their partner and education on prevention…”
1. Clinical Assessment
2. Investigations
3. Treatment
4. Education and prevention
Clinical Assessment
a. History
Current symptoms (local and systemic)
Itch, dysuria, discharge, pain, lesions, dysparenua, rash, joint
pain, conjunctivitis.
Sexual history
Past Hx of STI, PID, ectopic.
Risk factor grouping
Temp, rash, joints
Examine ext. genitalia
Lesions, D/C
Speculum exam
Cervix – D/C, lesions, take swabs
Bimanual Ex
Blue-topped swabs (vaginal and cervical) for D/C
Do wet film + culture
PCR high vaginal swabs
For viral – not really indicated
For Chlamydia PCR
Thin prep or urine PCR for Chlamydia
Serological tests for syphilis, HIV, Hepatitis (not Chlamydia – high background)
Chlamydia serology may be used in infertility Ix for ?PID.
Cameron Korb-Wells & Kai Brown (2009)
VDRL antibody test usually becomes positive 1-3 weeks after
chancre first appears. RPR is similar.
 False +ve 5-20%.
 May be raised in connective tissue diseases, infections (EBV,
leprosy, malaria) and pregnancy.
 May be raised in late latent phase or from congenital infection.
 Positive test should be confirmed with fluorescent antibody
Azithromycin 1g stat single dose
Doxycycline 200mg OD for 2/52 if PID (CI in pregnancy)
± repeat testing 2 weeks later.
Ceftriaxone 250mg IM single dose
Amoxycillin 3g + Probenecid 1g PO single dose
Should Rx for Chlamydia as well
Bacterial vaginosis, Trichomonas
–azole cream or PO
No cream during pregnancy.
always treat the partner where indicated
Education and prevention
Re: contact tracing, likelihood of recurrence, safe sex.
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to understand the aetiology and
management of the common female endocrine disorders.
Elicit, present and discuss the history of a patient with gynaecological disorders
Obtain menstrual, sexual, and obstetrical history; information on the type of contraception
used by the patient; results of past Papanicolaou (Pap) smears; records of previous
gynecologic procedures; history of discomfort during pelvic examinations; and history of pelvic
infections, infertility, endometriosis, or polycystic ovary syndrome. Review symptoms involving
pelvic pain, vaginal discharge, abnormal uterine bleeding, urinary incontinence, sexual
function, and infertility.
Recognise normal physical signs on pelvic examination
Pelvic examination consists of evaluation of the abdomen, external genitalia, internal
genitalia, and the rectum. Examination of the abdomen includes inspection, auscultation,
palpation, and percussion. Look for abnormalities of skin colour, hernias, organomegaly,
masses, fluid collection, and tenderness.
Inspect and palpate the external genitalia. Evaluate the hair distribution, skin, labia minora
and majora, clitoris, introitus, perineal body, Bartholin glands, and urethral meatus for
developmental abnormalities, discoloration, erythema, inflammation, excoriation, ulcers,
plaques, verrucous changes, rashes, masses, and evidence of trauma or infection. Palpate
for areas of tenderness. Observe cervix for any visible abnormalities though also obtain Pap
Bimanual examination includes palpation of the vagina, cervix, uterus and adnexae. Elevate
the organs using bimanual technique to determine the size, shape, symmetry, mobility,
position, and consistency of the uterus and ovaries.
Rectovaginal examination is to assess a retroverted uterus, to screen for colorectal cancer in
women 50 years of age or older, and to detect pelvic abnormality or disease.
Abnormal vaginal bleeding (investigations and management)
Types of abnormal bleeding
Leiomyoma, endometrial hyperplasia,
Endometrial, cervical (rarely vagina or
oestrogen-producing ovarian)
uterine bleeding
Primary bleeding disorders (vWD),
endocrine abnormalities
Diagnosis of exclusion. 90% due to
unopposed oestrogen in anovulation 
proliferative endometrium. 10% ovulatory
Endometrial cancer, vaginal atrophy,
exogenous hormones
TV U/S, sonohysterogram,
Endometrial biopsy, Pap
smear/ cervical biopsy, D&C
(gold standard)
Coags, endocrine tests (FSH,
Other causes must be ruled
>1 year after menopause.
Must rule out malignancy!
Characterisation: abnormalities in frequency, duration, volume and/or timing
o Menorrhagia: heavy or prolonged
o Metrorrhagia: intermenstrual bleeding
o Metromenorrhagia: heavy bleeding at regular intervals
Uterine fibroids: benign proliferations of smooth muscle in myometrium. Typically
women of childbearing years regressing during menopause. Generally only
Cameron Korb-Wells & Kai Brown (2009)
problematic when location results in heavy or irregular bleeding or reproductive
o Pathophys: monoclonal, varying in size from microscopic to size of full-term
pregnancy, hormonally responsive to oestrogen and progesterone. Classified
by location in uterus (submucosal, intramural, subserosal)  intramural most
common type, while submucosal associated with heavy bleeding. Large
amount of ECM and surrounded by pseudocapsule of compressed tissue/
SM. May outgrow blood supply  infarction, degeneration and pain
 Degenerative changes: hyaline, cystic, red (haemorrhagic), calcific,
Risk factors: non-smoking, multiparous, perimenopausal, hypertensive. Lowdose OCP generally protective.
Hx: asymptomatic (50-65%), abnormal bleeding  menorrhagia/ postcoital
spotting/ metrorrhagia/ menometrorrhagia. May lead to iron-deficiency
anaemia and weakness/ fatigue. Pelvic pain if vascular compromise present
(most common subserosal pedunculated) though secondary dysmenorrhoea
may occur, infertility 2-10%
O/E: nontender irregularly enlarged uterus with lumpy protrusions firm/ solid
on palpation
Ix: pelvic U/S most common, hysteroscopy, MRI may distinguish from
Rx: expectant though other causes must be ruled out (if growing, follow 6
monthly to assess size and growth). Rx if symptomatic.
 Medical: medroxyprogesterone, danazol, leuprolide  shrink with
decreasing oestrogen though resume growth on cessation
 Uterine artery embolisation: cause ischaemic necrosis, degeneration
and reduction in fibroid size  only for those not desiring pregnancy
 MRI-guided high-intensity ultrasound (expensive and not widely
available): thermoablation with high intensity ultrasound waves, for
premenopausal women completed childbearing and wish to retain
 Hysteroscopic myomectomy: symptomatic and wish to preserve
fertility, though recurrence in 50%
 Hysterectomy: definitive treatment
F/U: when hysterectomy not indicated, F/U to monitor size and location. If
obscures adnexae, Rx recommended. Rapid growth may be sign of rare
Dysfunctional uterine bleeding (diagnosis and management)
• If no pathologic cause identified, diagnosis of dysfunctional uterine bleeding (DUB) is
made. DUB is a diagnosis of exclusion.
Cameron Korb-Wells & Kai Brown (2009)
Anatomic lesions and systemic diseases must be excluded: blood dyscrasias, thyroid
dysfunction, malignancy, PCOS, endometriosis, PID, fibroids, unopposed oestrogen,
polyps, or pregnancy
> 90% DUB is due to anovulation; thus “anovulatory bleed” often used synonomously
o during anovulatory cycles, failure of ovulation results in lack of progesterone,
thus endometrium is exposed to prolonged unopposed oestrogen stimulation
 overgrowth of endometrium that breaks down and bleeds (irregular
oestrogen-dependent breakthrough bleeding), unaccompanied by normal
premenstrual molimina (premenstrual mood change, bloating, breast
tenderness, dysmenorrhea)
Remaining 10% due to dysfunction of corpus luteum – inadequate progesterone
Adolescent Age Group: immature hypothalamus with irregular LH, FSH, oestrogen
and progesterone pattern
Reproductive Age Group: DUB due to an increase or decrease in progesterone level
Perimenopausal Age Group: DUB due to increased ovarian resistance to LH/ FSH
Mid-Cycle Spotting: may be physiologic due to mid-cycle fall of estradiol
Premenstrual Spotting: may be due to progesterone deficiency, endometriosis,
adenomyosis and fibroids
o Exclude organic (systemic/anatomic) causes first!
o Ensure ß-hCG is negative
o If anaemic, supplement with iron
o OCP 1 tab tid for 10 days then 1 tab od for 4-6 months or
o medroxyprogesterone acetate (Provera) 5-10 mg od on first 10-14 days of
each month
o Replace fluid losses
o Medroxyprogesterone acetate (Provera) 10 mg for next 7-10 days
Acute, severe DUB:
o Oestrogen (Premarin) 25 mg IV q4-6h
o Endometrial biopsy (for diagnosis)
o D&C
o Endometrial ablation after pretreatment with danazol or GnRH agonists
o Hysterectomy
Postmenopausal bleeding
* vaginal bleeding >12 months since amenorrhoea after final menstrual period
Any postmenopausal bleeding is abnormal and should be investigated given the increased
risk of reproductive cancers in women of this age group. The most common cause of
bleeding, however, is endometrial and/or vaginal hypertrophy and not cancer. Endometrial
cancer only responsible for ~10-15% of all postmenopausal bleeding
My differential diagnosis of postmenopausal bleeding includes:
• Vaginal/ endometrial atrophy (30%)
• Exogenous oestrogens (30%)
• Endometrial cancer (15%)
• Endometrial polyps (10%)
• Endometrial hyperplasia (5%)
• Non-gynae: urethral caruncles, rectal bleeding (haemorrhoids, fissures, prolapse)
My approach to management includes:
• Focused history and examination to elucidate symptoms and identify any clinically
apparent cause of bleeding, including consideration of non-gynae bleeding (GI,
Cameron Korb-Wells & Kai Brown (2009)
Targeted investigations: centring around ultrasound evaluation of endometrial
thickness and homogeneity to assess risk of cancer, with further blood tests and
biopsy where indicated
Management of identified aetiology
History and examination
• Detailed history of menopause, symptoms and associated features very important
o Medications: tamoxifen may increase risk of endometrial cancer
• Examination
o Inspection: careful inspection of external anogenital region, vulva, vagina
and cervix
o Pap smear
o Digital rectal examination
• Ultrasound (TV): if endometrial stripe homogenous and uniformly <5mm, no further
evaluation generally required (risk of missing significant abnormality is very low, 0.1%
in HRT users and 1% in non-users)
• Bloods: FBC, TSH, PRL, FSH
• Tumour markers (if ovarian mass identified): LDH, hCG, AFP, CEA inhibin,
• Endometrial biopsy: ? should be performed to rule out cancer, regardless of other
identifiable source of bleeding
• Hysteroscopy/ D&C: in those with abnormal US findings or where persistent
bleeding despite normal US findings  diagnostic and therapeutic
• Treat causal agent
• Vulval/ vaginal lesions: biopsy and treat accordingly
o Vaginal lacerations: repair
o Vaginal atrophy: topical oestrogen (creams, pill, rings), HRT
• Endometrial polyps: remove with hysteroscopic resection or D&C
• Endometrial hyperplasia: progestin or hysterectomy
• Endometrial cancer: TAHBSO +/- lymph node dissection, RT or CT
Consider primary v secondary, as pathophys unique guiding DDx and management
 Primary: absence of menses in women who have not undergone menarche by age 16
or have not had menstruation by 4 years after thelarche
 Secondary: absence of menses for 3 cycles or a total of 6 months in women who
previously had normal menstruation
o *** most common cause of secondary amenorrhoea is pregnancy
1. Outflow tract anomalies
2. End-organ disorders
3. Central regulatory disorders
 Outflow tract anomalies
 Imperforate hymen: failure to canalise during fetal development, remaining as
solid membrane across introitus  if imperforate, will not allow egress of menses
o Hx: pelvic/ abdo pain from accumulation and dilatation of vault and uterus
with menses
o O/E: bulging membrane inside vagina, with purple-red discolouration
consistent with hematocolpros
o Rx: incision and hymen sewn open to allow egress of menses
Cameron Korb-Wells & Kai Brown (2009)
Transverse vaginal septum: failure of mullerian-derived upper vagina to fuse
with urogenital sinus-derived lower vagina. Commonly at level of midvagina,
usually patent though may be imperforate  primary amenorrhoea.
o O/E: may be mistaken for imperforate hymen, differentiate by presence of
hymeneal ring below septum
o Rx: resection of the septum
 Vaginal agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome): mullerian
agenesis/ dysgenesis and may have complete vinal agenesis and absence of
uterus or partial vaginal agenesis with rudimentary uterus and distal vagina.
o O/E: no patent vagina, PE exam  pelvic mass (uterus)
o Ix: karytope 46XX, ovaries on ultrasound, uterus on US/CT/MRI
o Rx: neovagina may be created by serial dilation of perineal body over
extended period or reconstructive surgery  may be connected with
upper genital tract
 Testicular feminisation/ androgen insensitivity syndrome: dysfunction or
absence of testosterone receptor with phenotypical female 46XY. ~1/50,000.
Testes present, may be undescended or to labia majora  mullerian inhibiting
factor produced and therefore no mullerian-derived structures.
o O/E: absence of pubic/ axillary hair (diminished testosterone sensitivity),
breast development (oestrogen), vagina ending in blind pouch
o Rx: neovagina for sexual function though unable to reproduce.
End-organ disorders
 Ovarian failure: low oestradiol but elevated gonadotropins, may arise from
variety of causes.
o Turner syndrome: rapid ovarian atresia and no primordial oocytes left
o Savage syndrome: receptor defect  failure to respond to LH/FSH
 Gonadal agenesis 46XY (Swyer syndrome) congenital absence of testes in
genotypic male  MIF not released and thus both internal and external female
genitalia though without oestrogen do not develop breasts
Central disorders
 Hypothalamic: deficiency in GnRH production, transport or pulsatile release
impairs pituitary gonadotropin release (hypogonadotropic hypogonadism)
o Kallmann syndrome: congenital absence of GnRH, associated anosmia
o Pituitary stalk disruption: impairs transport, may result from tumour mass
effect, trauma, sarcoidosis, TB, irradiation
o Other: defects in GnRH pulsatility in anorexia nervosa, extreme stress,
athletics, hyperPRL, hypothyroidism, rapid weight loss
 Pituitary: rare, usually second to hypothalamic dysfunction though may be
caused by tumours, infiltration of the pituitary or infarcts.
o Neurosurg/ irradiation: decrease or absent LH/ FSH
o Haemochromatosis: may deposit iron in pituitary  gonadotroph
Approach to management
 Clinically: work up on phenotypic picture
o Uterus: ? present
o External genitalia: ? patent vagina present
o Breast development: contingent on ovarian oestradiol secretion
 Ix: karyotype analysis, followed by testosterone and FSH assays  further
biochem and hormonal assays for specific enzyme defects
 Anatomic abnormalities: Asherman syndrome and cervical stenosis
o Asherman syndrome: intrauterine synechiae or adhesions, usually secondary
to intrauterine surgery or infection (D&C, myomectomy, C/S, endometritis)
o Cervical stenosis: scarring of cervical os secondary to surgical or obstetric
 Ovarian dysfunction: ovarian failure or PCOS
o Ovarian failure: from torsion, surgery, infection, chemo/radiotherapy though
premature failure often idiopathic. <35, chromosomal analysis to look for
genetic basis.
Cameron Korb-Wells & Kai Brown (2009)
*** Premature ovarian failure: menopause without other aetiology
before 40, considered
o PCOS (below): chronic anovulation with elevated oestrogen and androgens,
as well as reduced sex hormone binding globulin and increased LH:FSH
ratio, atypical follicular development, with cyclical propagation of disease.
Specific Rx below.
Hyperprolactinaemia: amenorrhoea and galactorrhoea, abnormal gonadotropin
release from alterations in dopamine levels with hyperprolactinaemia
o Aetiologies: primary hypothyroidism (TRH  increased PRL), medications
(dopamine antagonists, TCAs, oestrogen, MAOIs, opiates), PRL-secreting
pituitary adenoma
Hypothalamic/ pituitary dysfunction: secretion/ transport/ pulsatility GnRH
Approach to management
o Begin b-hCG to rule out pregnancy before formal history
o Hx: onset of symptoms, any of hypothyroidism, hyperprolactinaemia,
hyperandrogenism, medications
o O/E: visual fields, cranial nerves, breast (attempt express milk)
o Ix: TSH, prolactin, LH/FSH, progesterone challenge test if PRL normal, MRI
(rule out central lesion)
 Progesterone challenge test: 10mg PO 7-10 days  assess
adequacy endogenous oestrogen production and outflow tract.
Withdrawal after challenge indicates oestrogen and outflow thus
usually secondary to anovulation. Absence of bleeding should be
evaluated with oestrogen and progesterone administration. If still no
bleeding, consider outflow tract obstruction (Asherman/ cervical
o Mx:
Oligo-amenorrhoea / PCOS (cause and management)
 Most common endocrinopathy in reproductive age women, affecting 5-10%
 Rotterdam Criteria – two of three of:
o Oligo- and/or anovulation
o Clinical and/or biochemical signs of hyperandrogenism
o Polycystic ovaries (by ultrasound): 12 or more follicles in each ovary
measuring 2 to 9 mm in diameter and/or increased ovarian volume (>10 mL)
 Other aetiologies (congenital adrenal hyperplasia, androgen-secreting tumours,
Cushing's syndrome) must be excluded
 Pathophysiology: not fully characterised – combination of hypothalamic-pituitaryovarian axis dysfunction and insulin resistance. Combination stimulates ovarian
androgen production, with insulin resistance also impairing hepatic production of
Cameron Korb-Wells & Kai Brown (2009)
SHBG contributing to increased circulating free androgens. Dysregulation of follicle
regulation by androgens impedes normal growth, resulting in arrest at 4-8mm size.
Dominant follicle does not develop and ovulation does not occur
o Insulin resistance: insulin resistance and secondary hyperinsulinemia affect
~65-70% of women with PCOS. Many of these women are also obese, which
further exacerbates their insulin resistance. Insulin stimulates ovarian theca
cell androgen production and secretion, and suppresses hepatic production
of sex hormone-binding globulin. Increased intraovarian androgens then
disrupt folliculogenesis. Hyperinsulinemia may also directly cause premature
follicular atresia and antral follicle arrest
Management: lifestyle modification  insulin sensitisation where indicated 
ovulation induction  LH analogues  ovarian drilling
o Clomiphene: SERM (mixture of isomers enclomifene and zuclomifene)
 Mechanism: inhibits action of oestrogen on hypothalamus, binds
oestrogen receptors preventing normal receptor recycling, causing
effective reduction in hypothalamic oestrogen receptor number 
oestrogen no longer effectively feeds back on hypothalamus 
GnRH secretion more pulsatile  increased FSH/LH release
o Metformin: oral biguanide antihyperglycaemic
 Mechanism: activates AMP-activated protein kinase pathway (AMPK)
 ↓ gluconeogenesis, ↑ peripheral insulin sensitivity
o Clomiphene v metformin: Interest arose 1998, with several small RCTs over
subsequent years demonstrating significant benefit of metformin over
clomiphene in enhancing ovulation rates and menstrual cycling  larger trials
2006-2009, assessing live birth rate as primary outcome, found clomiphene
superior to metformin in isolation and no significant difference when
metformin added in combination with metformin
o Patients desiring fertility within the next few years may be considered for
metformin therapy
o Improve ovulation and cycling without the risk of higher order pregnancies
o Those desiring conception more rapidly should consider clomiphene or other
o Metformin may be beneficial over clomiphene in those with impaired glucose
tolerance and/or obesity
o Metformin may be used as an adjunct in women who are clomiphene
o Metformin offers favourable metabolic benefits over metformin during
pregnancy and beyond
Cameron Korb-Wells & Kai Brown (2009)
Hirsuitism/ severe acne (investigations and management)
• Hirsutism: excess hair with male pattern on the face, back, chest, abdomen, and
inner thighs, usually in response to excess androgens.
• Virilism: hirsutism, deepening of the voice, frontal balding, clitoromegaly, and
increased musculature.
• Primary causes: PCOS, ovarian tumors, adrenal tumors, CAH, and Cushing
• Diagnosis: history and physical, serum assays for testosterone, DHEAS, and 17OHP, and imaging studies.
• Management: primary treatment for the underlying cause; hormonal therapy with
OCPs, GnRH, or progestins; and cosmetic treatment of hirsutism.
Menopause management (risks and benefits of HRT)
Advice – from Woman’s Health Initiative RCT
• Menopause is a time when the woman’s body natural sex hormone (oestrogen)
production diminishes. HET aims to replace that oestrogen for a time whilst the
woman’s body adjusts to that change. Progesterone is also given (unless no uterus)
so that prolific effect of oestrogen on the uterus’ lining doesn’t go unopposed. These
doses are much lower than that in OCP (HRT ≠ contraception).
o Alternatives include vaginal oestrogen creams, phytoestrogens (~natural),
lifestyle changes.
• Treatment goals – improve symptoms of menopause (physical, mental, emotional).
Not recommended for prevention of some cancers or osteoporosis (exception –
sometimes used in women in 60-80yrs).
• Benefits
o ↓ risk endometrial and bowel cancer (small ↓ ~ 6 per 10,000)
 Risk of other cancers unchanged (except breast – below)
o Cognitive function – some observational studies suggest protective against
dementia, WHI suggested increased risk of dementia in elderly patients.
o ↓ risk of fractures (small ~ 5 hip # per 10,000)
o Improved survival in those with significant risk factors for CVD.
 If started <10yrs from menopause, CV events less likely
 If started >10yrs from menopause, CV slightly more likely, with most
risk in first year of therapy, but overall very small.
 No difference in CVD in oestrogen only group, slight non-significant
increase in stroke in this group.
• Risks
o Cancer
 HRT treatmet > 5 years, incidence of breast cancer ↑ 8 : 10,000 (not
statistically significant). Continues to increase with longer duration.
 Risk of breast cancer in women 50-70yrs who have never used HRT
is 45 : 1000.
 FHx of breast cancer does not increase risk caused by HRT.
 No increased risk in oestrogen-only group.
o Small increased risk of VTE (past VTE is a relative CI only)
o Risks not seen in women with early menopause, until age >50yrs.
• In most cases, woman who use HRT should continue screening for breast Ca as per
normal and are reviewed regularly to see if it is making a difference to QoL. The need
for HRT is reviewed at 5 yrs, sometimes with an HRT-free trial period. It is common
for women to continue taking HRT beyond 5 years with no problems
Premenstrual Syndrome (management)
PMS and more severe premenstrual dysphoric disorder are characterised by physical +/behavioural changes in second half of cycle. 75% of women recurrent PMS symptoms, with
30% of these having significant problems and 5% incapacitated or severely distressed by
PMDD. Highest incidence late 20s to early 30s.
• Symptoms: include headache, weight gain, bloating, breast tenderness, mood
fluctuation, restlessness, irritability, anxiety, depression, fatigue, and feeling of being
Cameron Korb-Wells & Kai Brown (2009)
out of control
o 2 weeks prior to menstruation
o At least 7-day symptom-free interval in first half of cycle
o At least two consecutive cycles
Pathophys: multifactorial physiologic + psychological. Recent studies suggest
interaction between serotonin and cyclic changes in ovarian steroids, with abnormal
response to normal hormonal changes (nb serum concentrations of E/P are the same
as those without problems)
Rx: several systematic reviews
o Exercise and relaxation
o OCP: most no effect though Yaz (with drospirenone with
antimineralocorticoid and antiandrogenic activity) effective for PMS
o Vitamin supplementation: some role for calcium, vit D, vit B6, magnesium
o Diet: carbohydrate-rich beverages improve both psych symptoms and
appetite cravings, modulating tryptophan (and serotonin) synthesis
o SSRI: treat both physical and mood symptoms  fluoxetine
o SNRI: venlafaxine
o Benzo: alprazolam
Dysmenorrhoea is pain and cramping during menstruation interfering with normal activities
requiring OTC or prescription medication (mild pain during menses is normal).
CONSIDER primary or secondary, AGE of patient and TIMING of pain
• Primary: idiopathic menstrual pain without identifiable pathology
• Secondary: painful menses due to underlying pathology (endo, fibroids,
adenomyosis, PID, cervical stenosis)
Primary: <20, usually diagnosed late teens (ovulatory cycles), arising from increased
endometrial prostaglandin production and psychological contributors
• Dx: Hx and absence of organic causes. Associated nausea, vomiting, headache. O/E
generalised pelvic tenderness.
st nd
o DDx endometriosis: though pain of primary dysmenorrhoea on 1 /2 day
menstruation cf endometriosis 1-2 weeks before menstruation worsening 1-2
days before and relieved at onset of flow.
• Rx:
o Non-pharm: heating pads, exercise, massage, acupuncture, hypnosis, TENS
o NSAIDs: first line, taken at onset of menses for 1-3 days and then prn.
o OCP: second line without adequate relief from NSAIDs or cannot tolerate.
>90% women relief with OCP in continuous (preferred) or cyclic fashion.
Mechanism cessation of ovulation or decrease endometrial proliferation and
PG production.
Secondary: symptoms secondary to identifiable cause (endometriosis/ adenomyosis,
fibroids, cervical stenosis, adhesions)
• Endometriosis: abnormal tissue growth resembling endometrium in locations other
than uterus, usually ovaries, pouch of Douglas and broad ligament. Associated with
premenstrual pelvic pain, causing symptoms by disrupting normal tissue, forming
adhesions and fibrosis and causing severe inflammation  severity of symptoms not
necessarily correlative with amount of endometriosis.
o Pathogenesis: 3 theories
 Halban: endometrial tissue transported via lymphatic system to
various sites in pelvis, where grows ectopically.
 Meyer: multipotential cells in peritoneal tissue undergo metaplastic
transformation into functional endometrial tissue
 Sampson: endometrial tissue transported through tubes during
retrograde menstruation, resulting in intra-abdominal pelvic implants
Cameron Korb-Wells & Kai Brown (2009)
Epi: ~10-15%, though surgical confirmation required therefore likely
significant underestimate. ~20% women with chronic pelvic pain and 30-40%
women with infertility
o Risk factors: first degree relatives  7x more likely, some associations with
autoimmune disorders
o Hx: cyclic pelvic pain beginning 1-2 weeks before menses, peaking 1-2 days
before onset and subsiding at onset of flow or shortly thereafter;
dysmenorrhoea; dyspareunia; abnormal bleeding; infertility
o O/E: signs may be subtle or nonexistent, to maximise examination yield
should perform during menses when implants likely largest/ most tender 
may have tender nodularity along uterosacral ligament +/- fixed retroflex
uterus or enlarged ovaries
o Ix:
 Laporoscopy gold standard with direct visualisation and biopsy
demonstrating endometrial glands
 Pelvic ultrasound: may be suggestive with endometriomas, etc
o DDx: other processes resulting in recurrent pelvic pain  PID, recurrent
salpingitis, adenomyosis, fibroids, adhesions, CL cysts, ectopic, ovarian
o Rx: dependent on symptoms/ age/ desire for fertility/ disease stage. Utilise
multidisciplinary approach with medical and surgical management as well as
pain center involvement and psychiatric support
 Minimal symptoms: expectant management
 Problem is infertility: operative laporoscopy to excise endometriosis
and restore pelvic anatomy. Medical management has no role in
patients trying to conceive, only delays surgical Rx which is shown to
improve conception rates
 Problem is pain: induce state of anovulation, either through inducing
a “pseudopregnancy” or “pseudomenopause”
• Mild pain  NSAIDs +/- continuous OCP, progestin’s (PO
and IM medroxyprogesterone)
• Mod/ severe pain  androgen derivative (danazol, though
androgen S/E) GnRH agonists (leuprolide) or SURGERY
 Surgical approaches: conservative or definitive
• Conservative: laparoscopy and fulguration of visible
endometrial implants, laparoscopic cystectomy
• Definitive: TAHBSO, lysis of adhesions and removal of
endometriosis lesions  where childbearing complete and
severe refractory disease
Adenomyosis: extension of endometrial glands and stroma within the myometrium.
Cause unknown - ? oestrogen-stimulated hyperplasia of basalis layer endometrium
and invasion of myometrium  diffuse globular enlargement of uterus with
hypertrophy and hyperplasia adjacent to ectopic endometrium. Most extensive fundus
and posterior uterine wall. As from basalis layer, does not undergo proliferative and
secretory changes cyclically, and is generally not responsive to regulation with OCPs/
other hormonal. Individual areas not circumscribed  boggy feeling on palpation.
o Epi: 15%, generally parous women late 30s-early 40s
o Risk factors: adenomyosis, endometriosis and fibroids frequently coexist. 1520% also endometriosis, 50-60% also fibroids.
o Hx: asymptomatic (30%), secondary dysmenorrhoea (30%), menorrhagia
(50%), dysmenorrhoea and menorrhagia (20%). Pain may begin up to 1
week before menses and last until cessation of bleeding. May complain of
bladder/ rectal pressure from enlarged uterus.
o O/E: diffusely enlarged globular uterus, 2-3x normal size. Softer and boggier
than firmer/ rubbery uterus with fibroids
o Ix: TSH, MRI most accurate tool (need to differentiate fibroids from
adenomyosis), pelvic U/S may be initial modality (with MRI if U/S suggestive),
hysterectomy provides definitive diagnosis
o Rx: dependent on severity of dysmenorrhoea and menorrhagia
 Mild symptoms: analgesia, NSAIDs, OCP, progestin’s
Cameron Korb-Wells & Kai Brown (2009)
Mod/severe: hysterectomy only definitive treatment, endometrial
biopsy should be performed to rule out endometrial hyperplasia or
carcinoma before hysterectomy performed
Uterine fibroids: as above in abnormal uterine bleeding
Cervical stenosis: congenital or secondary to infection/ trauma/ surgery
o Hx: scant menses with cramping pain relieved with menstrual flow
o O/E: scarring of external os, unable to pass uterine sound
o Rx: cervical dilation  surgical or laminaria stents (latter seaweed dilating
over 24 hour period absorbing water from surrounding tissue)
Pelvic adhesions: infections, inflammatory diseases or prior pelvic surgery
o Rx: antiprostaglandins, laporoscopy, laparotomy (if dense)  though surgery
produces further adhesions and pain
Chronic pelvic pain without pelvic pathology (causes and management)
Chronic pelvic pain is intermittent or constant pain of >6 months duration.
History and examination underpins diagnosis and treatment of CPP. Use of imaging such as
ultrasound and CT may not help diagnose the specific problem but is useful in excluding
structural pathology. Given dynamic relationship between different systems converging in
pelvis (GI, urological, genital), pathology may present with a variety of symptoms and often
considerable overlap between symptoms arising.
Background: Estimated to affect at least 15% of women 18-50. Women who present
with CPP symptoms may experience one or more of a diverse group of problems that
require correct diagnosis and appropriate treatment for the symptoms to be
o Gynae: endometriosis, adenomyosis, endosalpingiosis, adhesions, fibroids,
chronic PID, ovarian cysts
o GI: IBS, gastric outlet obstruction, chronic constipation, opioid bowel
syndrome, IBD, diverticulitis
o Urological: interstitial cystitis, terminal dysuria, chronic UTI
o Musculoskeletal: pelvic floor myalgia, myofascial pain syndrome,
visceromuscular reflex neuropathy
o Other: depression, drug-seeking behaviour, somatisation, fibromyalgia,
physical or sexual abuse
Risk factors: young age, smoking (dose-related effect), low BMI (<20), early onset
menarche (<12 years), premenstrual syndrome, heavy/ irregular menses, long
duration between cycles, PMHx sterilisation/ PID, psychological factors (anxiety and
Protective: regular physical exercise, omega 3 oils, OCP, young age at first
pregnancy, higher parity, stable relationship
o Pain: timing, onset, characteristics, location, distribution, severity (use VAS to
assess Rx)
 Upper boundary pelvic pain: umbilicus, with innervation of ovary from
 Lower boundary pelvic pain: knee, with obturator nerve passing
immediately below ovary and through obturator foramen to medial
thigh with somatic and motor innervation to inner thigh to knee
o Menstrual history
o Obstetric history: episiotomy, assisted vaginal delivery
o Sexual: risk factors for PID/ endosalpingiosis, history of sexual violence (30%
of CPP)
o PMHx: depression, other psych
o PSHx: pelvic surgery
o Meds: current and past treatment for pelvic pain
o Systems review: GI (problems with defecation), urinary (problems with
urination, with pain through/ at end of/ after voiding)
Cameron Korb-Wells & Kai Brown (2009)
General: posturing during history taking, facial pain characteristics
Vitals: hypertension, tachycardia, fever
Abdomen: scars, distension, masses, allodynia, inguinal haeniae/ lymph
 Constipation: may lead to palpable colon +/- pelvic pain, often in
those taking analgesia
 Carnett test: ask patient to lift head off bed to contract abdo wall
muscles --> abdo wall musculature pain increased, pelvic pain
maintained or decreased
Pelvic: empty bladder, perform U/A
 Inspection: dermatoses, vulval irritation, inflammation, discharge,
swabs if discharge
 Speculum
 Digital: less likely to provoke pain
• Assess muscles which should be elastic and non-tender with
contraction and relaxation (puborectalis first, pubocyccygeus,
coccygeus, piriformis and obturator internus)
• Assess anterior vaginal wall: pain along urethra, base of
bladder or trigone may indicate lower urinary tract
 Bimanual: note nodulatrity in uterosacral ligaments (endometriosis),
rectovaginal space --> nodules, faecal loading or tenderness
 Swabs/ Pap smear as indicated
* note allodynia of vulva, and trigger points in vulval skin
* visualise hymenal remant and posterior fourchette, assess
elevation of urethra/ vagina/ anus with contraction of pelvic floor
muscle contraction
Investigations: begin simple inexpensive
o Bedside: U/A, mid-stream MCS, vaginal swabs
o Bloods: as indicated
 FBC, CRP, CA125 most useful
 UEC, LFT, autoimmune second-line
o Imaging:
 U/S (TA and TV) to assess genital tract as well as tactile information
--> fibroids/ adenomyosis, adnexal disease, pelvic collections (only
show endometriosis if ovarian involvement)
 CT/MRI: as indicated
o Invasive:
 Cystoscopy, laporoscopy, colonoscopy
Management: CPP will often expose a woman to a prolonged pain state leading to
pathophysiology of its own, independent of, or coexisting with, index cause for the
pain. This combination can make diagnosis and treatment difficult and it is useful to
adopt a team approach to the patient with significant CPP
o Multidisciplinary care: GP, gynaecologist, urologist, gastroenterologist,
physiotherapist, chronic pain team, pain psychologist, alternative health
o Non-pharm: physiotherapy, pain psychology, exercise programs, relaxation,
o Pharmacological:
 NSAIDs, paracetamol: first line, may be very effective esp myofascial
 OCP: trial for hormone-sensitive conditions contributing, accounting
for significant proportion, monophasic for 3 months trial
 Opioids: reserve for refractory cases
 TCAs: amyltriptyline --> increase pain threshold, improve sleep
patterns, treat coexistant depression
 Gabapentin/ pregabalin: specialist care
Cameron Korb-Wells & Kai Brown (2009)
Benzodiazepines: muscle-relaxing, in women with muscle spasms or
GnRH analogues/ danazol
Cameron Korb-Wells & Kai Brown (2009)
1. Discuss the applied anatomy of the uterus, vagina and supporting
The uterus lies in the pelvis between the bladder and rectum. The normal position of the
uterus—whether anteverted, midplane, or retroverted—is maintained by the round ligaments.
The ligaments insert laterally, anterior to the fallopian tubes, and then plunge into the pelvic
sidewall. The round ligaments may be viewed as the roof of the broad ligament. The broad
ligament contains the blood supply, lymphatic channels, and nerves of the corpus uteri.
The ureter enters the pelvis by crossing over the bifurcation of the common iliac artery just
medial to the ovarian vessels, courses just below the insertion of the uterine artery (“water
under the bridge”) into the lower uterine segment. The lower uterine segment and cervix are
bordered anteriorly by the bladder and posteriorly by the rectum. Moving downward, the
surgeon encounters the utero sacral ligaments, which provide critical support to the uterus.
Laterally and downward the broad ligament joins the cardinal ligament until the
cervical/vaginal junction is reached.
The fallopian tubes emerge from the fundus and are in close proximity to the ovaries. The
mesosalpinx descends from the tubes. The ovaries are joined to the uterus via the uteroovarian ligament, and to the pelvic sidewall by the infundibulopelvic ligament. The
infundibulopelvic ligament contains the ovarian vessels.
Uterine Ligaments
4 paired sets of ligaments:
1. round ligaments: travel from anterior surface of uterus, through broad ligament, through
inguinal canal, terminating in the labium majus; keep uterus anteverted
2. uterosacral ligaments: arise from sacral fascia and insert into posterior inferior uterus;
important mechanical support for uterus and contain autonomic nerve fibers
3. cardinal ligaments: extend from lateral pelvic walls and insert into lateral cervix and
vagina; important mechanical support, preventing prolapse
4. broad ligaments: pass from lateral pelvic wall to sides of uterus; coursing through the
broad ligament on each side is the fallopian tube, round ligament, ovarian ligament,
nerves, vessels, and lymphatics
Arterial Supply
The uterine artery arises from the internal iliac artery, as do the cervical, vaginal, and other
collateral vessels.
Venous Supply
The veins follow a course analogous to the internal iliac vein. The ovarian artery and vein
course in a cephalad direction and have no pelvic origin.
Lymphatic Drainage
Coursing parallel to the internal iliac vessels, the drainage from the corpus uteri and cervix
ends in the deep pelvic lymph nodes. The drainage from the ovaries is in a cephalad and
midline direction, coursing to the periaortic nodes, adjacent to the inferior vena cava and
Uterus – endometrium, myometrium serosa
Cervix – Internal os, endocervical canal, external os, ectocervix, fornices
Cameron Korb-Wells & Kai Brown (2009)
Cameron Korb-Wells & Kai Brown (2009)
2. Discuss the aetiological factors of utero-vaginal prolapse
3. Explain the meaning of urethrocoele, rectocoele and the degrees of
uterine prolapse
4. Demonstrate an ability to examine a woman with utero-vaginal
prolapse and relate the history to the physical findings
5. List the types of management of utero-vaginal prolapse
Risk Factors
o Pregnancy
o Vaginal childbirth
o 1.2x risk with each subsequent NVD, assisted deliveries/episiotomy related
risk controversial
o Menopause
o Aging
o Hypoestrogenism
o Chronically increased intra-abdominal pressure
o Chronic obstructive pulmonary disease (COPD)
o Constipation
o Obesity
o Pelvic floor trauma
o Genetic factors
o Connective tissue disorders
o Hysterectomy
o Spina bifida
Pelvic organ support is maintained by complex interactions between the levator ani
muscle, vagina, ligaments and endopelvic fascia .
o Injury may be direct, neurological (? Pudendal nerve)
o May relate to smooth muscle dysfunction or CT abnormalities
Bladder/urethra and rectum ‘herniation’ imposing onto the vaginal wall causing a bulge.
Better to describe in terms of what is seen – ant./post. vaginal wall prolapse (loss of
rugae), lateral vaginal wall prolapse (maintain rugae), cervical prolapse…
Uterine Prolapse
Most commonly occurs as a delayed result of childbirth injury to the pelvic floor (particularly
the transverse cervical and uterosacral ligaments)
Unrepaired obstetric lacerations of the levator musculature and perineal body augment
the weakness
Attenuation of the pelvic structures with aging can worsen the prolapse
Stage I prolapse: the uterus descends only partway down the vagina
Stage II prolapse: the corpus descends to the introitus and the cervix protrudes slightly
Stage III prolapse: the entire cervix and uterus protrude beyond the introitus
Stage IV prolapse: the vagina is inverted
Cameron Korb-Wells & Kai Brown (2009)
“Uterovaginal prolapse can be associated with GU, GI and MSK symptoms and may result in
severe morbidity and reduced QoL. Thus a thorough assessment including Hx and Ex and a
discussion on treatment options is appropriate. My approach would be…”
1. History
a. Risk factors
b. Symptoms
i. Bulge
ii. Urinary
iii. Bowel
iv. Sexual
v. Pain
2. Examination
3. Treatment options
1. History
a. Risk factors
Obstetric Hx (number, mode delivery, complications)
Chronically raise intra-abdominal pressure (obesity, constipation, COPD)
Pelvic floor trauma
Other med – CT disease, spina bifida
b. Symptoms
Sensation of vaginal bulge (? Rectal/bladder)
Seeing or feeling vag/perineal bulge (? Vulvar or vaginal
Pelvic or vaginal pressure (pelvic mass)
Heaviness in pelvis or vagina (hernia, inguinal or femoral)
Incontinence (sphincter incompetence)
Frequency (detrusor overactivity)
Urgency (Hypoactive detrusor)
Weak or prolonged stream (Bladder outlet obstruction)
Feeling incomplete emptying (Interstitial cystitis)
Position change to start or complete voiding
Incontinence (sphincter distruption or neuropathy)
Hard straining to defecate (prolapse)
Digital evacuation (rectal hernia)
Splinting vaginal or perineum to defecate (pelvic floor
Dyspareunia (vaginal atrophy)
↓ lubrication (levator ani syndrome)
↓ sensation
Pain in vaginal, bladder or rectum (interstitial cystitis)
Pelvic pain (levator ani syndrome)
Lower back pain (may be MSK or pelvic)
Cameron Korb-Wells & Kai Brown (2009)
2. Examination
Woman in lithotomy position.
Examine external genitalia
o Atrophy, lesions, obvious prolapse (stage II-IV)
o May elicit anal reflex and bulbocavernosus reflex (next to clitoris) but
not sensitive.
o Ask woman to perform valsalva (cough)\
 Does it protrude beyond hymen?
 Is it ant/post/lat?
 Ask woman if this is similar to maximal extent of prolapse.
Vaginal Examination
o Insert split speculum along posterior wall.
 Note any bulge, its location and presence or absence or
o Rotate speculum 180 degrees to anterior wall
 Note any post. bulge, presence of peristalsis (enterocoele
rather than rectocoele).
o Bimanual pelvic examination
 Note any other pelvic pathology
 Pelvic floor musculature tone
3. Treatment
Treatment choice depends on;
o the type and severity of symptoms,
o age and medical co-morbidities,
o desire for future sexual function and/or fertility, and
o risk factors for recurrence.
Treatment should strive to provide symptom relief, but therapy benefits should always
outweigh risks.
o Vaginal pessary
 May be used instead of or in combination with surgical Rx.
o Pelvic floor muscle exercises (may limit progression, little good evidence but
zero risk).
Obliterative and reconstructive (mesh repair, suspension and fixation)
The simplest, most effective procedure is vaginal hysterectomy with
appropriate repair of the cystocele and rectocele.
If pregnancy is desired, a partial resection of the cervix with plication of the
cardinal ligaments can be attempted
For women who do not desire coitus, partial obliteration of the vagina is
surgically simple and effective
Cameron Korb-Wells & Kai Brown (2009)
6. Discuss urinary continence in the female
7. List and define the types of urinary incontinence
8. Discuss the aetiological factors of each type of urinary incontinence
9. Demonstrate an ability to diagnose the type of urinary incontinence by
taking a history and performing an adequate physical examination
10. Understand the basic principles of urodynamic testing
Infectious Symptoms
 Dysuria
Irritative (storage) symptoms
 frequency, nocturia, dysuria, urgency
Obstructive (voiding) symptoms:
 hesitancy, straining, intermittency, decreased force or caliber of stream, prolonged
voiding, post-void dribble, incomplete emptying
 stress incontinence, urge incontinence, incontinence without emptying (overflow),
 history of neurological problems, past pregnancies and method of delivery, past
abdominal-pelvic operations
Neurogenic bladder
 bladder normally can sense when full
o Afferent – pudendal nerve (somatic) and visceral para/sympathetic fibres
(sensation of fullness)
o Efferent
para S2-S4 > pelvic plexus > bladder and sphincter
Symp T10-L2 > hypogastric/pelvic plexus > bladder SM, sphincter +
proximal urethra
Somatic S2-3 > pudendal nerve > external sphincter.
 ‘Neurogenic’ bladder can be failure to store or failure to empty
Stress: urine loss with sudden increase in intra-abdominal pressure
(e.g. coughing or sneezing) ––> usually only lose a few drops of urine
 weakness of pelvic floor musculature (child bearing, previous abdominal/pelvic surgery)
 damage/weakness of urethra or sphincter (eg. hypoestrogen of menopause, child
 mechanism: proximal urethra drops below pelvic floor and transmission of increased
intra-abdominal pressure is not distributed evenly; pelvic floor supports weak (bladder
pressure > urethral pressure)
 Dx by stress test
 degrees: mild: sneezing, coughing; moderate: leaks when walking;
 severe: leaks when standing up
Urge: urine loss preceded by strong, unexpected urge to void
 local bladder irritation (e.g. cystitis, stone, tumour, infection)
 associated with inflammatory or neurogenic disorder
 urodynamics - uninhibited contractions if unstable bladder (detrusor hyperreflexia/instability);
 small bladder capacity if irritable bladder (“detrusor overactivity, overactive bladder,
neurogenic bladder”)
Cameron Korb-Wells & Kai Brown (2009)
Overflow: urine loss when intravesical pressure exceeds urethral pressure (due to
retention and overdistension)
 obstructive (e.g. BPH, stricture)
 hypotonic bladder (e.g. DM, autonomic neuropathy, anticholinergic meds)
 urodynamics: large bladder capacity
Functional: urine loss caused by inability to reach toilet in time
e.g. physical immobility
 history +/– voiding diary
 physical exam: GU, DRE, neurologic
 labs: urinalysis, urine C+S, renal profile
 other investigations:
o catheterization with post-void residuals
o U/S
o cystoscopy
o urodynamic studies – cystometrogram (CMG), uroflowmetry
Insertion of urinary catheter after attempt at complete void
Residual volume measured (send for M/C/S)
Measure pressures (in bladder ± urethra, rectum i.e. intraabdominal)
o Intravesical – intraabdominal = pressure exerted by bladder.
Measure flow rates
o Filling and emptying
Also has EMG readings
Cameron Korb-Wells & Kai Brown (2009)
After successfully completing the term you will be able to understand the nature of benign and
malignant lesions of the female reproductive systems and the significance of pre-malignant
conditions of that area so that you can identify those patients requiring further investigation
and can appreciate their management.
Aetiology and preventative factors in reproductive system malignancy
Incidence of malignant gynaecological lesions: endometrial > ovarian > cervical > vulval >
vaginal > tubal
Uterine cancers
Endometrial Ca
o Epi: 4 most common cancer in women, 2-3% women in lifetime, mean age
60 years, majority diagnosed early, >90% 5YS stage 1 disease, overall all
stages 5-year survival 60-70%
o Risk factors: unopposed oestrogen (obesity, PCOS, HRT), nulliparity, late
menopause, chronic tamoxifen use, oestrogen-producing ovarian tumours,
o Histopath: adenocarcinoma 80%, adenosquamous carcinoma 15%, papillary
serous adenocarcinoma 3-4%
o Spread: most commonly direct extension, transtubal dissemination,
lymphatic to pelvic/ para-aortic, haematogenous (lungs)
o Clin: postmenopausal bleeding 90% or abnormal uterine bleeding
o Ix: endometrial biopsy, D&C +/- hysteroscopy
o Rx: based on tumour grade and depth of invasion
 Surgical: TAH/BSO and pelvic washing +/- pelvic/ periaortic node
dissection; stage 1  TAH/BSO and washings, stages 2/3 
TAH/BSO and washings/ node dissection, 4  no surgery
Cameron Korb-Wells & Kai Brown (2009)
Adjuvant RT: selected patients based on invasion, grade and LN
 Hormonal: progestins for distant/ recurrent disease
 Adjuvant CT: if progresses
Uterine sarcoma: rare 2-6% uterine malignancies, arising from stromal components
(endometrial stroma, mesenchyme or myometrial), greater tendency for
haematogenous dissemination with 35% 5YS
Leiomyosarcoma: may rarely be associated with leiomyoma with similar
o Epi: uncommon, average age 55 years
o Path: histologic distinction from leiomyoma  increased mitotic count,
tumour necrosis, cellular atypia
o Clin: rapidly enlarging fibroid in postmenopausal woman
o Dx: usually postop after uterus removed for fibroids
o Rx: TAH/BSO, no adjuvant if confined to uterus and low mitotic index, RT if
high mitotic index, CT (25% response rate) if extrauterine spread
Endometrial stromal sarcoma
o Clin: perimenopausal women 45-50 with abnormal uterine bleeding
o Dx: histo from endometrial biopsy or D&C
o Rx: TAHBSO (always removing ovaries), progestins in low grade only
Mixed Mullerian sarcoma: 40% all uterine sarcomas, poorest overall survival
o Clin: postmenopausal bleeding 90%, soft to palpation, 1/3 polypoid tumour
through cervix
o Rx: as leiomyosarcoma, RT often used
Ovarian – LOTS!
• Approach to investigation of suspicious ovarian mass
o Bimanual examination: solid, irregular, fixed pelvic mass suggestive
o Ix: bloods and imaging
 Bloods: FBC, LFTs, UECs, CA-125 for baseline (though 50%
sensitivity, age influencing reliability of test as tumour marker)
• Other causes elevated CA-125: malignant and benign, gynae
and non-gynae
o Malignant: gynae  ovary, uterus; non-gynae 
pancreas, stomach, colon, rectum
o Benign: gynae  benign ovarian neoplasm,
endometriosis, pregnancy, fibroids, PID; non-gynae:
cirrhosis, pancreatitis, CRF
 Imaging: CXR, abdo/ pelvic U/S +/- transvaginal, CT or U/S to assess
urinary tract (NB bone scan not indicated)
 Rule out primary: occult blood (endoscopy +/- barium enema if
positive), gastric symptoms (gastroscopy +/- upper GI series),
abnormal PV bleed (Pap smear and endometrial biopsy rule out
concurrent endometrial/ cervical cancer), mammogram
• Screening ovarian cancer; no effective method, routine CA-125 not recommended,
controversial in high risk groups
o Starting 30, transvaginal U/S and CA-125 (non consensus on interval):
familial ovarian cancer (BRCA-1), other cancers (endometrial, breast, colon),
may recommend with BRCA1/2 prophylactic bilateral oophoretomy after age
35 or when child-bearing completed
• Benign tumours: mostly asymptomatic, usually slow growing, may rupture or torsion
 pain (usually originating iliac fossa radiating to flank) and peritoneal irritation may
result from infracted tumour
• Malignant tumours: see table
o Epi: in women >50, >50% ovarian tumours malignant, 4 leading cause of
cancer death in women
o Path: 65% epithelial, 35% non-epithelial, 5-10% epithelial have hereditary
o RF: nulliparity, early menarche/late menopause, age, FHx, race (Caucasian)
Cameron Korb-Wells & Kai Brown (2009)
Protective: OCP (? Ovulation suppression), pregnancy/ breastfeeding, tubal
ligation, hysterectomy
Clin: usually asymptomatic until disseminated, with most presenting as
advanced stage 3 disease
 Early: post-menopausal bleeding, irregular menses if premenopausal (rare), vague abdo symptoms (nausea, bloating,
dyspepsia, anorexia, early satiety)
 Late (mass effect): increased abdo girth (ascites or tumour), urinary
frequency, constipation
Ovarian tumours
• 4-8 cm mass,
unilocular lined
with granulosa
• if <6 cm, wait 6 weeks then reexamine as cyst usually
regresses with next cycle
• OCP (ovarian suppression) –
will prevent development of new
• treatment usually laparoscopic
• painful, multiloculated, or
partially solid masses warrant
surgical exploration
• larger (10-15 cm)
and firmer than
follicular cysts
• same as for follicular cysts
Tumours (all
Follicular cyst
• follicle fails to rupture
during ovulation
Lutein cyst
• corpus luteum fails to
regress after 14 days,
becoming cystic or
• due to atretic follicles
stimulated by abnormal
beta-hCG levels
Luteoma of
• usually bilateral
• due to prolonged
elevation of beta-hCG
• usually
• may rupture, bleed,
tort, infarct causing
pain ± signs of
peritoneal irritation
• more likely to cause
pain than follicular
• may delay onset of
next period
• associated with
molar pregnancy,
ovulation induction
with clomiphene
• conservative
• cyst will regress as beta-hCG
levels fall
• associated with
multiple pregnancy
• same as for theca-lutein
• regresses postpartum
• see Endometriosis
• see PCOS
Neoplastic ovarian tumours
• single most common
solid ovarian neoplasm
• elements of all 3 cell
lines contains dermal
appendages (sweat and
sebaceous glands, hair
follicles, teeth)
• may rupture, twist,
• 20% bilateral
• 20% occur outside of
reproductive years
• smooth-walled,
mobile, unilocular
• ultrasound may
show calcification
which is
• cystectomy
• may recur
• children and young
• aggressive, rapidly
growing, 2-3% of all
ovarian cancers
• produces lactate
• 10% bilateral
Benign cystic
Cameron Korb-Wells & Kai Brown (2009)
• surgical resection (often
conservative unilateral salpingooophorectomy) ± chemo, ±
• usually very responsive to
dehydrogenase (LDH)
chemotherapy, therefore
complete resection is not
necessary for cure
Yolk sac
• produces alpha
fetoprotein (AFP)
• rare
• unilateral
• produces AFP and hCG,
• produces hCG
• see GTN
unilateral salpingooophorectomy
malignant or
• derived from mesothelial
cells lining peritoneal
• 80-85% of all ovarian
neoplasms (includes
• varies depending
on subtype
• most common ovarian
• 50% of all ovarian
cancers (75% of epithelial)
• 70% benign
• 20-30% bilateral
• lining similar to
fallopian tube
• often multilocular
• histologically
bodies (calcified
• 85% benign (20% of
• rarely complicated by
peritonei: implants
seed abdominal cavity
and produce large
quantities of mucous
early (stage 1A &1B)
TAH/BSO + omentectomy +
peritoneal washings + staging
(peritoneal biopsy + node
cytoreductive (debulking)
If cannot remove, debulk to
residual disease <1 cm
combination (platinum + taxol)
Clear cell
• 20% of epithelial ovarian
• high malignant
• high malignant
• <1% of epithelial ovarian
• <1 % of epithelial ovarian
• majority benign
• resembles
• often
• may reach
enormous size
• histology
but non-invasive
radiation in patients with no
residual disease (rare)
If mucinous - remove appendix
as well
• histology
mesonephric cells
• fibrotic tumour
with transitional
• cell–like
epithelial core
Sex Cord
Cameron Korb-Wells & Kai Brown (2009)
• from mature fibroblasts in
ovarian stroma
Granulosatheca cell
(benign or
• can be associated with
endometrial cancer
cell tumour
(benihn or
• non-functioning
• occasionally
associated with Meig’s
• estrogen-producing –
–> feminizing effects
(precocious puberty,
menorrhagia, postmenopausal bleeding)
• androgen-producing
––> tumours (benign
virilizing effects
(hirsutism, or
malignant) deep voice,
recession of front
• firm, smooth
rounded tumour
with interlacing
• histologic
hallmark of cancer
are small groups
of cells known as
Call-Exner bodies
• surgical resection of tumour
• chemotherapy not effective for
from GI tract,
• 4-8% of ovarian
• Krukenberg
tumour =
metastatic tumour
from GI tract
(usually stomach)
with “signet-ring”
• Benign lesions
o Nabothian cyst/ inclusion cyst  no Rx required
o Endocervical polyps  polypectomy (office procedure)
• Malignant lesions
o Squamous cell carcinoma (95%), adenocarcinoma (5%)
o Average age 52
• Aetiology: at birth lined with sqamous epithelium, during puberty oestrogen
stimulates eversion of single columnar layer (ectopy) exposing it to acidic pH of
vagina leading to sqamous  columnar metaplasia. Metaplastic squamous
epithelium covers columnar epithelium and new squamocolumnar junction formed
closer to external os. TZ is area of squamous metaplasia between original and new
squamocolumnar junction. Majority of dysplasias/ cancers arise in TZ.
• Risk factors
o HPV infection: high risk 16, 18; low risk 6, 11  99% cancers at least one
high risk HPV type
o Smoking
o High risk behaviour: multiple partners, other STIs, early age first intercourse,
high risk male partner
o Low SES
• Pathophys: dysplasia  CIS  invasion (slow process over years, growth by local
extension with late metastasis)
• Prevention: quadrivalent HPV recombinant vaccine Gardasil
o HPV types 6, 11, 16, 18
o Full benefit: administer before onset of sexual activity
o Administer IM at 0, 2 and 6 months
o Avoid conception for 30 days after last dose
o s/e: pain, swelling, erythema, low grade fever
• Clinical features
o SCC: exophytic, fungating tumour
o Adenocarcinoma: endophytic with barrel-shaped cervix
o Early: asymptomatic, discharge (watery  brown/ red), post-coital bleeding
Cameron Korb-Wells & Kai Brown (2009)
Late: 80-90% with bleeding (postcoital, postmenopausal or irregular),
spontaneous irregular bleeding, pelvic/ back pain (extension to pelvic walls),
bladder/ bowel symptoms
o Signs: friable, raised, redenned area
Screening guidelines: see below
Abnormal Pap smears in pregnancy: incidence 1/2,200
o Pap at all initial prenatal visits: if abnormal refer to colposcopy
o If diagnostic conisation required defer until 2 /3 to prevent abortion
o Microinvasive Ca: follow to term and deliver vaginally or by CS depending on
o Stage 1B: depends on patient wishes, T1  EBRT with expectation of
spontaneous abortion; T2  delay therapy until viable fetus and delivery
o Follow-up with appropriate Rx
• Benign: malignant potential <5%, greatest risk when cellular atypia on biopsy
o Non-neoplastic
 Hyperplastic dystrophy (squamous hyperplasia): surface thickening,
pruritis, postmenopausal, Rx 1% fluorinated corticosteroid ointment
 Lichen sclerosis: diminished subepithelial fat, thin labia, labial fusion
 pruritis, dyspareunia, burning  Rx topical steroid
 Mixed dystrophy (both of above): hyperkeratotic with areas thin/
shiny epithelium  Rx fluorinated corticosteroid ointment
o Tumours
 Papillary hidradenoma: apocrine sweat glands, cystic lesion
ulcerates and becomes necrotis
 Nevus
 Fibroma
 Haemangioma
• Malignant: 5% genital tract malignancies, 90% SCC, remainder melanomas/ BCC,
usually post-menopausal
o RF: HPV, vulvar intraepithelial neoplasia (white/ pigmented plaques)
o Clin: most asymptomatic, most on labia majora, then labia minora 
localised pruritis/ lump/ mass
o Ix: physical examination, BIOPSY, +/- colposcopy
o Prognosis: depends on nodal involvement, >3cm poor prognosis, 5YS 79%
• Benign
o Inclusion cysts: from abnormal healing of laceration  Rx nil
o Endometriosis: bleed at menses  Rx excision
o Gartner’s duct cysts: remnants of Wolffian duct  Rx conservative unless
o Urethral diverticulum: may produce recurrent UTI/ dyspareunia  Rx
surgical if symptomatic
• Malignant
o RF: HPV, prior cervical/ vulvar cancer
o Ix: Pap smear (10-20% false negative), colposcopy, Schiller test (normal
epithelium takes up iodine), biopsy, partial vaginectomy, staging
o SCC:
 Epi: 80-90% vaginal cancer, 2% gynae malignancy, mostly upper 1/3
posterior vagina, 5YS 42%
 Clin: asymptomatic (painless discharge/ bleeding), vaginal discharge
(often foul-smelling), postcoital bleeding, urinary +/- rectal symptoms
 Rx: RT if primary, hysterectomy and vaginectomy
o Adenocarcinoma
Cameron Korb-Wells & Kai Brown (2009)
Epi: most metastatic from cervix/ endometrium/ ovary/ colon, most
primaries clear cell adenocarcinomas
 2 types: non-DES and DES syndrome
 Rx: as for SCC
DES syndrome: maternal use and fetal exposure DES  cervical/ vaginal
clear cell carcinoma
 Clin: adenosis if persistant Mullerian glandular epithelium (1/1000
develop clear cell cancer), occurs 30-95% exposed females
• Congenital malformations: upper vagina, cervix and interior
uterus (T shaped), cervical collar and pseudopolyps
 Rx: patients with DES exposure should have annual pap smears, any
abnormality  colposcopy
Cervical smear and knowledge of other techniques to diagnose malignant and premalignant lesions of the female reproductive system
Cervical cancer screening program aims to reduce incidence and death from cervical cancer,
in a cost effective manner, through an organised approach to cervical screening. Current
national policy in Australia is:
• Every 2 years for women with no symptoms or history suggestive
• Sexually active women commence between ages of 18 and 20 years, or 1-2 years
after first intercourse, whichever later
• Cease age 70 years with 2 normal smears within 5 years. >70 never had a smear or
who request a smear should be screened
Unsatisfactory smear
Repeat smear in 6–12 weeks, with correction, when possible, of problem that caused
the unsatisfactory smear
Low-grade squamous intraepithelial lesions (LSIL)
HPV testing: insufficient evidence to support HPV testing in triage of LSIL
Index Pap report LSIL: manage same way irrespective of whether possible or
definite  repeat Pap test in 12 months
Index Pap report LSIL age 30+: if no history of negative smears in preceding 2-3
years  either immediate colposcopy or repeat Pap in 6 months
12-month repeat Pap after index LSIL:
o Any changes: colposcopy
o Normal: repeat in 12 months (ie. 24 months after index smear)
Fluctuating results: colposcopy if two LSIL/possible LSIL within 3-year timeframe,
irrespective of intervening normal reports
Colposcopic assessment
o Normal: annual smears until 2 normal smears obtained, then routine
o High-grade lesion: targeted biopsy for histological confirmation, definitive
o Low-grade lesion: target biopsy, treatment of histologically confirmed LSIL
not recommended (just productive HPV infection)  repeat smear 12 and 24
 If both negative, return to routine screening
 If either LSIL: annual smear until at least 2 negative
o Unsatisfactory: repeat Pap 6-12 months, no further diagnostic procedures in
asymptomatic women in absence of cytologic, colposcopic or histologic
suggestion of high grade disease
High-grade squamous intraepithelial lesions (HSIL)
Cameron Korb-Wells & Kai Brown (2009)
Pap report HSIL: colposcopy and targeted biopsy
o Histo confirmation of high-grade lesion required before definitive treatment
Pap HSIL with features of invasive component: colposcopy, gynae oncologist
referral within 2 weeks
SCC: gynae oncologist for urgent evaluation within 2 weeks
Rx CIN 2/3: should be treated to reduce risk of developing invasive carcinoma
o Fertility-sparing: local ablative or excisional treatments should destroy or
remove tissue to depth of at least 7mm  no clearly superior method of
fertility-sparing treatment for CIN2/3
o Ablative therapy: if assessed by experienced colposcopiest, targeted biopsy
has confirmed diagnosis, no evidence of invasive cancer, entire TZ visualised
and no evidence of glandular lesion
o Cryotherapy: advisable that CIN3 not treated with cryotherapy
o LEEP: may create diathermy artefact obscuring path examination of margin
o Cone biopsy: absolute indications, though tailor to woman taking into
account size, extent and severity of lesion
 Failure to visualise entire TZ with HSIL on referral
 Suspicion of early invasive cancer
 Additional glandular abnormality
Once treated:
o Colposcopy and smear 4-6 months post-Rx
o Smear and HPV typing 12 months post-Rx
o Annual smear and HPV typing until both tests negative two consecutive
o Return to routine screening
Glandular abnormalities
Adenocarcinoma: referral to gynae oncologist
Endocervical adenocarcinoma in situ: colposcopy, referral to gynae oncologist
Possible high-grade glandular: colposcopy
Atypical glaundular/ endocervical cells underetmined significance: colposcopy
Colposcopy: mandatory when smear suggests glandular lesions
o Cold-knife cone biopsy gold standard for glandular lesions
o Cone/ punch biopsy: if smear report adenocarcinoma in situ  if invasive
adenocarcinoma found, refer gynae oncologist
Rx adenocarcinoma in situ: dependent on age and fertility requirements and status
of excision margins
o Hysterectomy recommended: difficulties in smear follow-up, high
recurrence rate and multifocality of disease
Abnormal Pap
o Low grade: repeat smear 12 months
o High grade: colposcopy
o Aim: exclude invasive cancer and reassure pregnancy not affected by
abnormal Pap test  biopsy unnecessary unless invasion suspected
Rx HSIL: defer until after pregnancy if not invasive
No matter grade: colposcopy as cytology surveillance alone inadequate
Evaluate whole lower genital tract, as same risk factors for cervical/ vaginal/ vulval/
perianal lesions
Cameron Korb-Wells & Kai Brown (2009)
Rx: excisional methods
F/U: colposcopy AND smear, annual and indefinite
Management strategies of malignant lesions of the female reproductive system
o Leukoplakia
 Topical corticosteroids
• S/E: mucosal thinning, absorption
 PUVA, methotrexate, cyclosporin
o VIN seen with 5% acetic acid (6% go onto cancer, linked with HPV)
 Wide local excision or laser ablation
o Carcinoma (95% are squamous, rare, occur in elderly mainly)
 Stage 1 and 2 (<2cm, no nodes)
• ‘triple incision’
• or radical vulvectomy + wide excision + inguinal nodes
• may need skin grafts
o Regular Pap smears (2 yearly if normal)
o Abnormal pap smear:
 3 types:
• ASCUS: Atypical squamous cells of undetermined significance)
o Follow up pap smear in 6 months
• Squamous intraepithelial lesions
• Squamous cell carcinoma
 If suggestive of CIN 1 (inflammatory cells, or mild atypia)
• Repeat pap smear in 6 months
• Or Colposcopy if 2 repeat +ve
 If suggestive on CIN 2/3 or cancer
• Colposcopy
o Abnormal tissue has characteristic blood vessels and
stains white with acetic acid
o Punch biopsies taken for histology
o Doesn’t detect adenocarcinoma
o CIN 1 (mild dysplasia)
 Repeat pap smear 6 months
 50% return to normal
 serial pap smears (6 monthly), colposcopy if continue to be abnormal.
 Takes 7 years on average to progress to cancer
o CIN 2/3 (moderate dysplasia) (98% curable)
 Small lesions confined to exocervix:
• Cryotherapy
• Laser
• Electrocautery (requires laser)
• Repeat colposcopy, papsmears
 Endocervix
• Surgical excision of the transformation zone
o Cone biopsy
o Loop (LEEP) Electrosurgical Excision procedure
o Smear taken of tissue deep to that of biopsy and
margins checked
 95% SCC, 5% adenocarcinoma
 Stage 1 (tumors confined to cervix) – (80% 5 yr survival)
• Consider cone biopsy to maintain fertility for microinvasive
• 1A1- simple hysterectomy
Cameron Korb-Wells & Kai Brown (2009)
• 1A2 and 1B - radical hysterectomy
Stage 2 (local invasion beyond cervix but not beyond pelvic wall,
involves vagina but not lower third)
• TAH (60%- 5 yr survival)
 Stage 3 (Spread to pelvic wall and lower 1/3 of vagina)
• Extensive radiotherapy and chemotherapy
• TAH (up to 50% survival?)
 Stage 4
• Palliation
Endometrial cancer
o Surgical staging
o Peritoneal washing
o Pelvic aortic node sampling
o Local or regional radiation
o (stage 3 and 4 also: hormonal therapy and chemotherapy)
o 90% are epithelial tumors:
 TAHBSO, omentectomy, debulking procedures, taxol and cisplatin
based chemotherapy
o Germ cell tumors
 Removal of affected ovary, combination chemotherapy
Prognosis of common malignant neoplasm of the female reproductive system
See above.
Counselling of a patient with a malignant lesion of the reproductive system
Cameron Korb-Wells & Kai Brown (2009)