lOMoARcPSD|17581840

Obs& Gynae full summary notes

Medicine (Queen's University Belfast)

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OBSTETRICS

OBSTETRIC EMERGENCIES Amniotic fluid embolism:

 RARE
Shoulder dystocia:  Liquor enters maternal circulation – anaphylaxis with
 1/200: Normal downward traction failed to deliver shoulders sudden SOB, hypoxia and hypotension +/- Sz and cardiac
after head; damage to brachial plexus – Erb’s palsy (50% arrest (acute HF?)
remain) – waiter’s tip posture  If mother survives >30min – pulmonary oedema ARDs and
 Risk factors: Large baby or obese mother; diabetic mother; DIC. (PAD)
past Hx, 40+wk, long 1st or 2nd stage with IOL or oxytocin or  Risk factors: Rupture of membranes in labour or CS or
instrumental termination of pregnancy; strong contractions in
 TURTLE SIGN – pulled back into perineum polyhydramnios
Management:
Management: - Resus ABC and supportive Rx with O2
- Rapid & senior intervention. - Fluids under intense CV monitoring.
- Gentle downward traction AND episiotomy. - Bloods for FBC, U+E and coagulation factors.
- Drop bed with mother flat. - ICU admin
- Assistant to help the hyper-flexion and abduction of legs
onto abdomen (McRoberts manoeuvre) with suprapubic
Uterine rupture:
pressure over posterior aspect of anterior shoulder.
 1/1500
- Internal manoeuvres – insert hand behind anterior
 New tear or opening of old scar
shoulder and push it towards chest – RUBIN II
 Acute fetal hypoxia and massive internal maternal
- Combine with pressure on posterior shoulder to aid
haemmorhage.
rotation – WOODS SCREW
(If on lower transverse scar on lower segment, not as
- Attempt to rotate baby in other direction – REVERSE
vascular and less blood loss)
WOODS SCREW. Delivery of posterior arm, hand into
 Risk factors: Labour with scarred uterus from classical
vagina in front of posterior shoulder and swing arm in
Caesarean section or deep myometecomy
front of the chest.
 Diagnosis: Cessation of contractions, PV bleed, constant
- Patient moved to all 4s – increase AP of inlet
lower abdominal pain, maternal collapse with abnormal
- Symphsiotomy
FHR
- Head pushed back into vagina and then section and
Management:
intention fracture of clavicle.
- Resus ABC
- Last resort – Caesarean section– ***HELPER***
- Bloods (FBC, coag and G+Cx) and IV fluids.
o Help
- Urgent laparotomy for delivery of fetus and repair or
o ELevate leg  episiotomy
removal uterus.
o Pressure suprapubically
- Elective early CS for next pregnancy.
o Enter vagina for shoulder rotation (RUBIN II)
o Reach for posterior shoulder/ Return head into
vagina (Zavanelli maneourve)/ Rupture clavicle
or pubic symphysis Epileptiform Seizures:
Cord prolapse:  Aetiology: maternal epilepsy or eclampsia.
 1/500: Rupture of membranes & UC below presenting part;
risk of cord compression/spasm with infant becoming  Management:
hypoxic. Airway cleared +/- suction. Ox and cardiopulmonary resus.
 Risk factors: Preterm; breech; abnormal lie; multiple If no CV collapse – DIAZEPAM.
pregnancy; polyhydramnios If Eclamptic MgSO4
 Diagnosis: Abnormal FHR & cord palpated PV; appears at
introitus ALSO remember:
o Local anesthetic toxicity
Management: o PE
Push back the head with finger or tocolytics (terbutaline – o Uterine inversion
don’t want to touch cord and induce a spasm. If outside o Massive PPH or APH
introitus, keep warm and moist; on all 4 position and
immediate caesarean section.

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ABNORMAL LIE BREECH PRESENTATION

Longitudinal lie is normal Cephalic presentation is normal
OBLIQUE or TRANSVERSE LIE  Presentation of buttocks – extended breech (70%), flexed
breech (15%), foot long breech (15%)
AETIOLOGY:  NO CAUSE
o More room to turn:  Common associations with prematurity; twins; fetal or
- Preterm labour uterine abnormalities; placenta praevia; pelvic tumours or
- Polyhydramnios deformities; previous breech 8%
- Higher parity (more lax uterus)  Presentation: Asymptomatic or upper abdominal
discomfort.
o Prevention of turning:  Complications: Neurological handicap
- Multiple pregnancy
- Fetal or uterine abnormalities (1) ECV (50% success with 3% turning back) with no anesthetic
o give anti D, as it is a sensitizing event
o Prevention of engagement: o CTG monitor and Tocolytics (terbutaline) to reduce
- Placenta praevia uterine tone.
- Uterine deformities o Don’t do ECV if ***FTPAP***
- Pelvic tumours - Fetal compromise
- Twins
 Associated risk of cord prolapse or uterine rupture. - PROM
- APH recently
Management: - Placenta praevia.
 No action if <37/40. o More difficult to preform in prim obese Caucasian
 Admit after as risk of SROM. USS for cause. women
 If spontaneous version persistent for >48hrs can discharge.
Caesarean section delivery. (2) Elective caesarean section
(3) Vaginal breech birth, common with epidural. Don’t
encourage pushing until head visible. More difficult with >4kg
and fetal compromise.

Obstetric terminology

o Para: no of term pregnancies

o Para + x: no of pregnancies miscarried <24wk
o Nulliparous: never delivered a potentially live baby,
however may have had a miscarriage or an abortion
o Multiparous: woman who has delivered at least one baby
>24wk.
o Gravidity: no of times pregnancy (including this one)

APGAR SCORING

Trimesters of pregnancy:
1st trimester: 1-12wk
2nd trimester: 13-27wk
3rd trimester: 27-40wk

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LABOUR Monitoring progress in labour:

- Descent of fetal head in pelvis (not shoulders)
 POWERS  Contracts 45-60 secs/2-3 mins causing Cx - Increased frequency and length of contractions
effacement and dilatation - Cx dilation and effacement

- Colour of liquor& change in fetal heart rate doesn’t

 PASSAGES  Flexion and engagement, followed by
descent from contractions. Internal rotation and
extension. External rotation (restitution). Expulsion
with anterior then posterior shoulders, then legs.
Ischial spines are palpated vaginally to assess level of
descent.
- Station 0 = head at
spines
- Station -2 = 2cm below
- Station +2 = 2cm above
 Cx softening and dilatation
allows descent.

 PASSENGERS  Attitude is the degree of flexion.

Anterior and posterior fontanelle; vertex between.
Vertex presentation ideal 9.5cm. Brow presentation
13cm too large. Best presentation at OA.

 Sutures allow bones to slightly overlap to reduce head

diameter (moulding) which may result in localized
swelling (caput)

 Description of fetal head: presentation, presenting

part, position of head, attitude

 Initiation of labour with involuntary uterine

contractions (BRAXTON HICKS). Prostaglandin
decreases Cx resistance and increase oxytocin.
 Stimulation of contractions – more painful
contractions, dilation and effacement of Cx +/- show
+/- rupture of membranes.
 May also complain of backache, severe abdominal
pain, indigestion and diarrhea.

 1st stage until fully dilated and effacement. Descent,

flexion and internal rotation. Latent phase up to 20hrs,
active phase 4-5/10 lasting 45secs of increased length,
strength and pain
 2nd stage until delivery. Passive until head reaches
pelvic floor and pushing desire. Pressure ow on rectum
and perineum (purple line from bottox). Active
pushing, desire to bear down. 40 min prim/ 20 min
parous
 3rd stage delivery of placenta. 15min approx. 500mls
blood loss. Syntometrine IM.

 Signs of placental separation: lengthening of cord/

rush of blood PV
Normal Management of labour: Pain relief options in labour:
 Epidural/ spinal
 Preparation at antenatal classes
 Back rubbing or TENS machine
3 Water birth
 Inhalation of ENTANOX (mix of NO + O2) SE: sedation,
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 Regular observations (hypotension with epidural Rx: IVF +/- ephedrine. Hypertension Rx: labetalol)
 Mobilize regularly (squat, kneel, left lateral)
 Hydration (water or IVF if prolonged)
 Discourage eating (risk of aspiration – Mendelson’s syndrome - ?GA needed later. Give RANITIDINE)
 Pyrexia common if prolonged labour or epidural. If >37.5 increased risk of neonatal illness or chorioamnionitis. >38
increased risk of sepsis and give antibiotics.
 Monitoring essential:
o VE: cervical dilation and head descent
o Inefficient uterine action: slow progress (common in older, prim and IOL), however if too slow – augment, ARM,
oxytocin, empty bladder, give fluids of pain relief needed
o Hyperactive uterine action: strong, frequent or prolonged. Association with ++oxytocin (give tocolytic –salbutamol
IV or SC) or placental abruption.

BISHOPS Score of <5 = IOL needed

o Dilation
o Length
o Station
o Position
o Consistency

Risks of IOL:
o Increase chance of operative delivery
o Increase risk for complex analgesia
o Uterine hyperstimulation
o Uterine rupture (old
scar)

Countraindications to Propess:
o Active heart or lung
disease
o Previous caesearaean
section or multiparous
o Placenta praevia
o Malpresentation
o Fetal distress

Refusal of IOL at T+14:

o Twice a week CTG and
assessment of AF
volume

ABNORMAL LABOUR
(6) Poor progress in 2nd stage
(1) Uterine activity:  Secondary uterine inertia
 <4-5/10 – common in prim/ older women - made worse by epidural
 Monitor on tocograph and intrauterine pressure catheters - Full dilatation causes weak contractions and can
 Hydrate, pain relief and support be associated with dehydration or ketoacidosis
 Poor progression examine 2hourly - Give oxytocin
 ARM and oxytocin – need CTG monitoring  Rotation
 If oxytocin for 4 to 6 hours with no progression – CS  Small mid pelvis (ANDROID pelvis) – deep transverse
arrest as cannot rotate

(7) Multiple pregnancies

4 CS if mal-presentation of the 1st, 2nd twin bigger, IUGR,
placenta praevia, request.
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(2) Cephalo-pelvic disproportion:

 Small women <1.6m, previous fracture or bone disease
 Fetus: obstructive hydrocephalus, fetak thyroid, neck tumour
 Can give OXYTOCIN to prim, but never parous if suspected
 True vs positional CPD (failure to progress sometimes due to positional CPD of OP/OT)
 Suspicion if:
- Slow progress despite adequate contractions
- Fetal head not engaged
- On VE - severe moulding and caput
- Head poorly applied to Cx

(3) Birth canal: – fibroids and cervical dystonia (doesn’t dilate due to scarring)

(4) Abnormal lie:

Longitudinal, oblique and transverse

- More room to turn: -preterm labour/ polyhydramnios/ higher parity (more lax uterus)
- Prevention of turning: multiple pregnancy/ fetal or uterine abnormalities
- Prevention of engagement: placenta praevia/ uterine deformities/ pelvic tumours
 Associated risk of cord prolapse with risk of SROM/ uterine rupture.
 See above for Mx (ECV +/- tocolytics, CTG and anti D injection) if breech.

(5) Mal-presentation
 More common in parous and can cause ruptures
 Exclude cephalo-pelvic disproportion
 Failure of presenting part to engage and descend
 Excessive moulding
 Deep transverse arrest (no rotation, head in OP)

 BREECH – risk of prolapsed cord, CTG abnormalities with compression, mechanical difficulties can damage organs

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FETAL MEDICINE
 Prenatal scanning for age related trisomies, PMHx of trisomy, maternal request

(1) 1st trimester

- Booking scan at 11-14wks
- Combined test – nuchal scan and biochemical markers: PAPP-A and bHCG (85-90% detection)
- Nuchal translucency in the nuchal fold more prominent in T21. Measure NT/ FHR and CRL alongside maternal age and
ethnicity to calculate RISK  80% detection rate, 5% false rate
- Harmony test (NIPT) from 10wk in England – detection of T21 >99.9% - free fetal DNA in maternal serum
Combined test in 1st trimester Quadruple test in 2nd trimester
(2) 2
- Increased NT - Decreased AFP, oestradiol and PAPP-A n
- Increased b-hCG - Increased b-hCG and inhibin d
- Decreased AFP and PAPP-A
trimester
- Quadruple test for t21 – AFP, oestradiol, b-hCG, inhibin with 90% detection and 5% false +ve
- Soft markers on anomaly scan such as increased nuchal fold, renal pelvic dilatation

DOWNS SYNDROME
 6/1000 live births, greater risk 35+
 Random non-dysjunction at meiosis. 6% balanced chromosomal translocation in parents.
 Features:
o mental retardation
o Characteristic facial features with apparent macro-glossia (due to low tone), abnormal teeth, slanted eyes, flattened
nose
o Short neck and hands with OSA association
o AVSD
o Duodenal atresia and exomphalus
o Poor eustachian tube function with OME and associated hearing problems
o Greater risk of epilepsy, ALL, thyroid disease and early onset dementia.

Chorionic villous sampling- 98% detection

 Biopsy trophoblast through AAW/ cervix into placenta. 11 to 13wk, 2% risk of miscarriage
 Risk of placental mosaicism
 Ix: FISH and full karyotype

Aminocentesis - 99% detection

 Aspiration of amniotic fluid. 14+wk
 Risk of culture failure, placental mosaicism
 Late aminocentesis has risk of pre term labour – PROM, pulmonary hypoplasia, Rh iso-immunization and 1% miscarriage.

Fetal blood sample (CORDOCENTESIS) - at 20wk

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FETAL GROWTH PROBLEMS

 Failure to reach growth potential; constitutionally small or pathological

 EFW <10% or >2.5 SD below mean  SFGA/ IUGR
 If early delivery anticipated give Mg SO4 and steroids
 Prevention in future pregnancies with ASPIRIN
 Future complications for child: T2DM, obesity, hypertension and IHD

Causes of SFGA: Under 10th decile or <2.7kg at birth  **SWAN**

 Starved IUGR (SHIT) NORMAL:

 Wrong dates
 Abnormal (chromosomal or structural)
 Normal (CMPCCMP)
-
 Presentation: Reduced fetal movements and
growth slowing down.
 Investigations: USS. Doppler screen, surveillance
and differentiation.
 Uterine artery Doppler in
risk from 20-24wk  aware
severe notching in
abnormal waveform
 Umbilical artery Doppler
helps time delivery: absent
with insufficiency; reversed
needs delivered.
Causes of IUGR **SHIT**
Failure to reach growth potential.
Growth is slowing down
 Multiple pregnancies
 Congenital uterine anomaly
 Multiple fibroids
 HIGH RISK **SHIT** are
MATERNAL CAUSES
- Smoking and drugs
- HTN, disease, extremities
age
- IUGR previously
- Twins
o Constitutionally small fetus in primigravida, some ethical
groups (50%)
o Maternal RF (BMI, DM, smoking, drugs, fibroids)
o Pregnancy related (IVF, multiple pregnancy)
o Chromosomal abnormality (symmetrical <2th centile)
o Congenital infection (TORCH – toxoplasmosis, rubella, CMV
and herpes)
o Maternal disease (pre-eclampsia, SLE)
o Placental insufficiency (asymmetrical & brain sparing
Symmetrical IUGR (25%) Asymmetrical IUGR (75%)
high
Constitutionally small Placental insufficiency – lack of nutrients. of
Uterine abnormalities
Multiple pregnancy
Chromosomal abnormality SMOKING**
Congenital infection TORCH Non pregnancy related disease (SLE) and maternal disease
EDF
FAS UNKNOWN (50%) EDF
Management: Management:
o Confirm dates As symmetrical Mx and..
o Check ethnicity of parents, Fetal growth parameters, environment and Doppler to TIME
and BMI details DELIVERY
o Weight of previous babies Reduce maternal medical problems and screen for pre-eclampsia
o Fetal structural scan for
anomalies and ECHO (If there is redirected blood flow to the brain. Fetal renal blood
o USS: AFI flow decreased, hence oligohydramnios, decreased umbilical
o CTG flow. Placental infarction and necrosis from reduced nutrients.)
o Maternal TORCH screen 1) Umbilical artery Doppler: shows increased resistance
o Alcohol and drug in placental vessels. Reduced EDF indicates resistance.
Absent EDF. Reversed EDF indicates fetal hypoxic risk –
counselling
o DOPPLER USS: normal then needs delivered.
2) MCA Doppler: increased velocity with brain sparing.
continue and deliver >38wk
Indicates fetal anaemia
3) Venous Doppler: cardiac decompensation via ductus
venosus.
of
Give steroids if <37wk aiming for 37wks with regular Doppler’s.
Weekly scans if normal Doppler. Alternative days if absent EDF.
Delivery if reversed EDF

 Fetal alcoholic syndrome, congenital and TORCH infections = FOETAL CAUSES

 Complications: Hypoglycaemia, polycythaemia, NEC, RDS or intraventricular haemorrhage, cerebral palsy

Measurements on USS include:

- BPD (biparietal diameter)
- HC (head circumference) = microcephaly <5th centile; hydrocephalus >95th centile; doliocephaly (oval shape)
- TCD (transcerebellar diameter) = early fetal growth restriction sign <24wk
- EFW (estimated fetal weight) using the hadlock stem (BPD-AC-FL) used to plot growth and determine Mx.
- These growth charts look at parity, ethnicity and BMI of mother at booking scan.

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Polyhydramnios:
Antenatal monitoring:  Fetal abnormalities (NTDs, bowel atresia)
(1) USS assessment of fetal growth: Look at the rate of  Infection
growth by comparison with previous scans.  Hydrops +/- IUGR
Symmetrical or asymmetrical.
o Important in high risk or multiple pregnancies Oligohydramnios:
(2) Doppler umblical artery waveform: placental  IUGR
dysfunction with reduced end diastolic flow.  Pre-PROM (poor lung development increasing risk of RDS and
o Small fetus: growth restricted or limb contractures)
 Potters syndrome (renal agenesis)
compromised?
 Hydronephrosis and VUR due to obstruction
(3) Doppler waveforms of fetal circulation – MCA: sign of
fetal anaemia via increased velocity reflecting head
MEASURE AFI in all 4 quadrants
sparing
(4) CTG

FETAL ABNORMALITIES FETAL RHESUS DISEASE

Risk of HYDROPS FETALIS (fluid in 1+ body compartment)
 Exomphalos  worse prognosis. Partial extrusion in SAC.
50% chromosomal problems (including T21) o Scalp oedema on USS (enlarged BPD and HC)
 Gastroschesis  Free loops of bowel in cavity. Associated o Abdominal ascites
with cannabis and ectasy use. Risk of other genetic o Skin oedema
problems. o Cardiomegaly
- Investigation: Colour flow doppler differentiates; cord - Presents with reduced fetal movements (4 days
runs to the side in gastroschesis. before true hydrops develops)
- Increased risk of still births.
 Diaphgramatic hernia  leading to pulmonary hypoplasia. - Other causes include: structural, genetics,
 Oesophageal atresia, TOF and polyhydramnios infection (parvovirus), unknown
 Duodenal atresia and polyhydramnios double bubble
sign. Common in T21.  Management:
o Anti D Ab and other anti-E, anti-c, anti-Kell etc.
 Spina bifida  Failure of closure of neural tube at day 16. o Monitor titres in maternal serum.
Due to low folate in diet. RF: obesity, poor control DM, o MCA Doppler for monitoring fetal anaemia
epileptic meds. o Intrauterine Transfusion Therapy in Glasgow –
(1) Spina bifidia occulta – hairy patch, dimple, dark spot top up or exchange therapy. Remove 20ml at a
(2) Meningocele – sac of fluid at gap in spine time; check Hct to decide exact amount. Risk of
(3) Myelomeningocele – most severe, poor ability to walk, overload heart failure in neonate, preterm
bladder and bowel problems labour, fetal bradycardia leading to IUFD.
 Risk of associated ventriculomegaly <34wks do it every 2wks until 36wks then
 Prevention with folic acid two months pre-pregnancy then deliver
0.4mg/day for three months.
 Recurrence NTDs in 1 in 10 pregnancy, hence increase
dose. NEONATAL RHESUS DISEASE

 Anencephaly  Failure of bones to form at skull vault -  Anaemia

absent cranium and ‘frog eye’ appearance  Hyperbilirubinaemia
- ‘Lemon sign’ with fronted point of skull, ‘banana sign’  Kernicterus
with abnormal cerebellum  Deafness
 Encephalocele  protrusion of brain contents through
skull defect.
 Hydrocephaly (increased CSF, increased pressure)
 Cleft lip
 Polydactyly
 Hydronephrosis and VUR (can be unilateral or bilateral)
 Meconium ileus (association with cystic fibrosis)

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PRETERM DELIVERY PREVENTION:

1. Cervical cerclage: insertion of 1+ sutures to strengthen and
 24-37wks are preterm. keep cervix closed. Performed pre-pregnancy if history at 12-
 <34wk carries greater risk and <24wk usually miscarry. 14 weeks. Regularly scanning and sutured if shortening
 Iatrogenic (eg. pre-eclampsia) or spontaneous. (rescue suture)
2. Progesterone supplementation: suppositories pre-
AETIOLOGY: pregnancy.
o Myometrium stretch 3. Infection: Rx for STI or UTI or BV
o Cervical weakness and incompetence 4. Fetal reduction
o Infection in 60% 5. Rx for polyhydramnios – Amnio-reduction with needle
aspiration or provide fetal surveillance. NSAIDS decrease
 Screening: fetal UO and can cause reversible closure of ductus
o Cervical length (offered if PMHx or cervical treatment arteriosus.
under TVUS) 6. Rx maternal medical disease

Presentation: Painful contractions (50% stop spontaneously and Complications:

normal). Cervical incompetence with painless dilatation and dull
supra-pubic ache and increased discharge +/- fluid loss indicates NEONATAL MATERNAL
ROM Cerebral palsy Infection (-endometritis)
Signs: Fever and dilated cervix. Chronic lung disease Common post CS complications.
Blindness via ROP (retinopathy
 Investigations: of prematurity)
o Abdominal exam for presentation.
+/- minor disability (<24 wks.
o CTG or USS to assess fetal state 30% handicap/ 30% die)
o Fetal FIBRONECTIN or PARTASURE assay (+ve in labour;
helps time need for steroids) MANAGEMENT:
o TVS of cervical length. (>15mm increased chance) (1) Admit initially and observe
o Vaginal swab for infection (2) Steroids (Betamethasone) and tocolytics (Terbutaline – only
o Increased CRP and WCC with chorioamnionitis (?however use for 24 hours) if Fibronection +ve or short cervix
also raised with steroids) 2 dose of 12mg betamethasone IM, given 24 hours apart
Caution in DIABETICS to adjust insulin; chorioamionitis or
Risk factors for spontaneous pre-term labour: other maternal systemic infection
Mode of action of steroids: Maturation of type II
Previous Hx of preterm or late Lower SE pneumocytes to increase surfactant.
miscarriage >14wks (3) Monitor BG in diabetics +/- Nifedipine or Atosiban (oxytocin
Extremities of age Shorter inter-pregnancy interval receptor antagonist) to prolong action.
Multiple pregnancy Congenital fetal abnormality (4) Detect infection and treatment with antibiotics in ACTUAL not
Uterine abnormalities (including Pre-eclampsia or HTN threatened labour, as can cause long term cognitive
fibroids) impairment.
Polyhydramnios STI or vaginal inf
Immediate delivery if chorioamnionitis
UTI High Hb
o U SOFT
Bacterial vaginosis (GBS, TV, CT) Diabetes or thyroid
Cervical surgery o Uterine tenderness, severe lower abdo pain,
offensive or coloured liquor, fever, tachycardic
(5) MgSO4: neuroprotective to neonate.
(6) Transfer to tertiary NICU
(7) Delivery: vaginal reduces chance of RDS however, caesarean
section needed with breech.
(8) Clamp cord >45secs and antibiotics for GBS

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Pre- PROM

 Before labour <37wks.

 Complications:
o Infection of fetus/ placenta (Chorioamnionitis) or
cord substance (Funisitis).
o Absence of liquor <24wk can lead to pulmonary
hypoplasia and postural deformities.

 Presentation: Gush of clear fluid (normal) then further

leakage.
 Signs: Fluid pool in posterior fornix on speculum. DVE
excludes cord prolapse.

 Investigations: USS for reduced liquor. HVS. FBC/ CRP. Gram

stain for infection. CTG monitor.

Management:
o Admission and steroids
o Start erythromycin OD for 10 days
o OR close maternal and fetal surveillance
o IOL @ 36wk
o IV AB and delivery if chorioamnionitis.
(Antibiotics: Benzylmethypenicillin)

Check is it amniotic fluid with AMNISURE (99.7% accurate)

Differential diagnosis:
o Vaginal discharge
o Urine

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Early pregnancy signs

o Nausea and vomitting

o Increased micturtion and nocturia
o Breast tenderness
o Prominent montgomery tubercles
o Hyperpigmention: linear alba, nipple and areola
o lethargy

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Routine visit checks:

DIABETES
Maternal complications
Increased insulin requirements.
Hypo risk/ DKA rare
INFECTION: UTI or wound
infection or endometritis
o USS
o FBC
Fetal complications
o Blood group and antibody screen
Congenital defects – NTDs or
cardiac (control at conception o Urinalysis and MSU
important to avoid this) o Random CBG
o HIV and rubella status, syphilis and hepatitis screen
Increased UO & o HbA1c, U&E, LFTs are key
polyhydramnios; Increased
BW – MACROSOMNIA
(pancreatic islet cell hyperplasia
– hyperinsulinaemia – fat
dependent)

Pre-eclampsia Sudden fetal death/distress

IHD worsens Fetal lung immaturity and

RDS (due to suppression of fetal
cortisol production and more
common in prematurity)

Diabetic nephropathy has worse Dystocia and birth trauma

outcome; however no worsening
of it; Retinopathy worsens

Increased likelihood of caesarean Neonatal electrolye

section and birth canal trauma imbalances: hypoglycaemia,
hyperbilirubinaemia, hypoCa

 SMASHER
Fasting glucose >7.0 and GGT >7.8/2hr after 75g glucose
Shoulder dystonia
load. Macrosomnia
Abruption
Insulin requirement almost doubles as: Still birth
Hypoglycaemia
- Placenta secretes insulinase (degrades insulin),
- Decreased sensitivity to insulin dueprE-Eclampsia
RDS
to O and P effect
- Increased cortisol and human placental lactogen
- Increased calories with reduced exercise, brings an
increased glucose load.

 Increased risk of miscarriage and congenital

abnormalities (heart defects, NTDs)
 Increase in maternal glucose, increases fetal glucose
levels, increasing fetal insulin
 Increased fat deposition; binding to heart and liver
causing cardio and hepatomegaly

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GESTIATIONAL DIABETES Management of GD:

- Diet control and exercise 1st line
- If insufficient, metformin aiming for 6.5mmol/L.
 GDM detected in 2-9% in the 2nd trimester when all
- Insulin if higher FG.
hormones rise.
- 2 weekly check with HbA1c and U&E with diabetoligist,
 Hormones (HPL, cortisol, GH, progesterone) increased,
obstetrician and dietician.
increasing glucose production. There is reduced insulin d
uptake from increased peripheral insulin resistance.
Physiological to ensure fetus receives more glucose from
decreased maternal uptake
 B cell hyperplasia in pregnancy means increased insulin to
target cells for uptake to decrease glucose levels so they
don’t get too high.
 Increased insulin resistance in GDM, hence more glucose
into fetal circulation, increased fetal production of insulin
and increase uptake and fat deposition leading to
macrosomia.
 Macrosomia, malposition, hypos common. 20-50% go on
to develop T2DM, infections and HTN

Increased risk factors for developing GDM:

o Ethnic groups
o 1st degree relative with T1DM
o PMHx GM
o PCOS
o Maternal weight >90kg (BMI >30)
o Previous baby >4kg
o Previous unexplained still birth
o Glycosuria on 2+ occasions in this pregnancy
o Polyhydramnios (greatest pool >10cm)
o Fetal macrosomnia

 OGTT 75g at 24-30wks NOT urine (as raised GFR)

- Fasting >5.6 and >7.8/2hr

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HYPERTENSION IN PREGNANCY
 BP= CO x SVR Pre-eclampsia
 WCC increased , clotting factors & Hb diluted with  Multisystem disorder.
platelets decreased.  Progressive & variable
 Decrease 2nd trim by 30/15mmHg from decreased SVR –  Hypertension usually precedes ++proteinuria (0.3g/24hr)
SM relaxation and vasodilatation due to increased  6% prim; 15% recurrence rate.
progesterone; increase by term (normal)  Risk factors:
 CO increased by 50% (mostly in 3rd trimester) o Obesity
 GFR increased up to 40%, glucouria, reduced gut motility o Extremities of age
and thyroid enlargement o Chronic HT
 Utero-placental circulation increased. o Renal disease or DM
o FHx or PMHx
Pregnancy induced HTN Pre-existing/chronic HTN
o Multiple pregnancy

o >140/90 AFTER o >140/90 BEFORE  STAGE 1: Development  Normally trophoblastic invasion
20wk 20wk; already Dx through decidua and myometrium to infiltrate spiral
& on medication. arterioles & vasodilation. There is remodeling of these
o + PROTEINURIA o 1/2° causes arterties normally, with increasing vascularity and tortious
(>0.3g/24hr) = Pre- channels
eclampsia There is incomplete invasion; altered immune response?
Reduced uteroplacental BF – poor oxgen supply to
o Risk of o Risk of super- placenta - ischaemia
epileptiform Sz/ imposed pre-
eclampsia eclampsia  STAGE 2: Manifestation  Placenta releases
Gestational HT: IOL @ 40wk inflammatory factors locally altering circulatory function
 Mild pre-eclampsia: IOL @ 37wk
 Moderate to severe pre-eclampsia: IOL 34-36wk with
conservative Mx in specialist unit with NICU.
 Severe with complications and fetal distress – deliver
Risk factors:
o Age >40
o HTN >10yrs
o BP >160/110 in early pregnancy
o Diabetes mellitus
o Cardiomyopathy; CT disorder
 SMOKING protective against pre-eclampsia

Pre-existing HT
 HTN increases late in pregnancy
 Asymptomatic
Risk of super-imposed pre-eclampsia (always do
URINALYSIS check for proteinuria)  2+ admit and
do PCR/24hr or 1+ review in 2 days
 Investigations: U&E, TFTs, cortisol, BP in both arms.
 Management of pre-existing HTN:
o Counsel pre-pregnancy
o Change meds to Labetalol (combined a and b
blocker) or methyldopa
o May not need meds 2nd trimester (16-18wk)
with physiological decrease.
o Low dose aspirin 75mg to high risk mums before
16wk.
o UAE Doppler at 23wk.
Fulminating pre-eclampsia:
Management of pre-eclampsia:  Presentation: oedematous, HTN, proteinuria, renal and
liver failure as HELLP and DIC

14COMPLICATIONS: early onset; increasing chance in 24hr

postnatally
 Eclampsia
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 LABETALOL aiming for 140/90

 Oral nifedipine or IV labetalol 2nd line for initial control
 Outpatient management. BP and urinalysis every 2 week. USS every 2-4wk.
 Admission if severe HTN >160/110 and proteinuria or no HTN and ++proteinuria.
 MgSO4 – IVI for eclampsia prophylaxis. Slows neuromuscular conduction and increases perfusion with no effect on BP.
 Risk of toxicity (respiratory depression/hypotension – preceded by loss of patellar reflex – test regularly 15mins)

 Antedote (if respiratory drepression of loss of reflexes) is 1g CALCIUM GLUCONATE

 Prophylactic steroids if <34wk

 Monitor: hourly RR, O2 sats and deep tendon reflexes

 Monitor hourly urine output (if <20ml/hr STOP)
 Strict monitoring input and output. Catheterization if UO <50ml/hr
 Fluid restriction 83ml/hr
 If UO low  do a CVP
o High CVP: overload. Rx: furosemide
o Low CVP: need fluids.
o Normal and oligura: likely renal failure. If hyperkalaemia need dialysis

 BP series every 5min; check reflex (clonus 3+) if ?eclampic

Management in labour:
 If <34wk C.section with steroids 24 hours before.
 If >34wk: IOL with PROPESS.
 Epidural will reduce BP. Monitor BP and CTG.
 Avoid pushing if BP >160/110 in 2nd stage (Risk of Increased ICP and cerebral haemorrhage)

 Caesarean section if:

o Seizure
o Severe complication
o Cervix unfavorable
o Fetal compromise
o Preterm
 CLASSICAL CS if lower segment not formed (never can have NVD again)

OXYTOCIN in 3rd stage (NOT ERGOMETRINE as will increase BP further)

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HORMONAL CHANGES IN PREGNANCY Human chorionic gonadotrophin (hCG)

 Detectable in maternal serum from time of implantation
 Maintains the corpus luteum and progesterone production until
Progesterone the placenta takes over.
 Produced by corpus luteum until 35 days post conception;  Levels peak at 11wks, before declining
placenta thereafter.  Rate of increase indicative of the health of the pregnancy
 Maintains uterine lining
 Enlargement of breast lobules and myoepithelial contraction for Human placental lactogen (hPL)
the expulsion of milk  Stimulates mammary growth and maternal production of caesin,
 Decreases smooth muscle tone: lactalbumin and lactoglobulin
 In uterus, reducing miscarriage (by no contractions)  Anti-insulin actions in promoting GH release, promote its
 GI tract increasing constipation and GOR secretion but decreasing peripheral effects and liberates maternal
 Ureters increasing urinary stasis and infection FA, sparing maternal glucose.
 Raises body temperature  Increased glucose uptake, increasing fetal uptake for growth

Oestrogen Placental thyrotrophin

 Placental estradiol accounts for 90% of oestrogens in pregnancy  Stimulates maternal thyroid; maternal goiter due to increased
 Induces breast and nipple growth – colloid production. Thyroxine levels increase 2-3 times (TSH
increased adipose tissue in breast and reliable indicator)
lactiferous ductal system
 Water retention
 Protein synthesis
 Increases oxytocin receptors in the
uterus

Dual action: oestrogen and progesterone

 Breast enlargement and areolar pigmentation
 Uterine hypertrophy (x20)- lower segment forms at 28wk
 Increased PV discharge
 Cervical gland hypertrophy and thick mucous plug
 Vaginal lactobacilli proliferation increasing lactic acid; deceases
pH (protective layer to infection)

HAEMATOLOGICAL
PHYSIOLOGICAL CHANGES IN  Increased plasma volume 40% and RCC 25%- dilution of Hb
PREGNANCY 
hence anaemia
Increased clotting factors: hyper coaguable state and need
Hormones are needed to maintain pregnancy, prepare for delivery and
VTE prophylaxis
post partum period.
 Increased WCC

RESPIRATORY
MUSCULOSKELETAL
 Enlarged uterus, increased intra-abdominal pressure,
 Increased BMI
increasing diaphragmatic breathing
 Lower back pain (common. Physio and advice with lifting,
 Hyperventilation and increased TV (yet normal RR)
posture and firm mattress)
 Lordosis
CARDIOVASCULAR  Carpal tunnel syndrome and sciatica
 Increased CO (increased BF to placenta), increasing HR and  Muscle cramps
SV. Decreased SVR also increases SV, hence CO  Pelvic girdle pain: discomfort in pubic or sacroiliac joint.
 Reduced BP in 2nd trimester Physio and analgesia

GASTROINTESTINAL ENDOCRINE
 Gastro-oesphageal reflux  Increased activity in anterior pituitary gland, increasing
 Hemorrhoids hormone secretion.
 Constipation from decreased gut motility (worsens with oral  Oestrogen, progesterone, b-hCG, HPL, TSH (goiter)
iron. Encourage high fibre intake and stool softeners)
DERMATOLOGICAL
UROLOGICAL  Skin pigmentation – striae gravidarum
 Increased renal BF 40% - icreased GFR, hence reduced  Spider naevi from distension or proliferation of BV
creatinine and urea  Facial flushing
 Urinary frequency
 Increased kidney size and hydronephrosis

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Respiratory disease in pregnancy

PRE-EXISTING MATERNAL DISEASE  Normal meds safe.
Cardiac disease in pregnancy  Long-term steroids may need increased dose in labour –
 Common ejection systolic murmur in pregnancy chronically suppressed adrenal cortex and increase stress
 No epidural if AORTIC STENOSIS (suppresses BP) here.
 Risk of HF during labour.
 Thrombo-prophylaxis – LMWH Epilepsy in pregnancy
 Check for anaemia.  1/3 get better or no change or worsen.
 Increase risk of obstetric complications, especially pre-
MANAGEMENT:
eclampsia.
 Elective forceps delivery;
 Higher rates of congenital malformations
 Antibiotics in labour (artificial valves) ?endocarditis risk. - NTDs (4%) and epilepsy (3%) in children
 Peripartum cardiomyopathy rare. - Dysmorphic features: medial eyebrow deficiency, flat
nasal bridge, shallow philtrum, button nose, thin lips
ASPIRIN IN PREGNANCY from +ve pregnancy test or booking - Neuro delay: associated with cognitive and behavioral
scan at 12wk:  Seizure control can decrease throughout and in labour.
 >40 years Lamictal or Tegratol advised. Folic acid 400mcg and 5mg
 Interval of 10 years for high risk pre conception.
 BMI >35  General advise: when taking baths
 Previous HTN or IUGR  Give vitamin K from 36wks.
 FHx pre-eclampsia  Valproate has a high risk of NTDs, cleft palate,
 Recurrent miscarriage or thrombophilia hypospadias, ASDs and lower IQ
 DM

GBS
INFECTIONS IN PREGNANCY o HIGH MATERNAL carrier rate
CMV o Severe neonatal illness
o 1% maternal infection rate; 40% vertical transmission o Intrapartum PENICILLIN if high risk or +ve 3rd trimester
o Diagnosis with maternal IgM and IgG; fetal diagnosis screen
amniocentesis 20wk GAS
o Deafness common o Common cause of sore throat (or chorioamnionitis,
o Screening of vaccination. No treatment. puerperal sepsis)
Rubella o Supportive Rx and PENICILLIN
o Most female immune. Very rare
o Fetal infection <16wk Herpes zoster virus
o Screening identifies if need postnatal immunization o Many immune. Severe maternal illness in pregnancy
o <20wk occasionally teratogenic or if infection just before
Toxoplasmosis** (cat litter) delivery give IgG to neonate
o 0.2% maternal infection rate HepB
o Low % fetus permanently affected o High transmission rate and high chronic disease/mortality
o Screening NOT ROUTINE in UK to neonate.
o Diagnosis with maternal IgM; fetal amniocentesis 20wk o Screening and neonate needs Ig
o Treatment: spiramycin, fetal combo Rx
Syphillis HepC
o Rare o High risk. 6% vertical transmission
o Screening routine as Rx prevents congenital syphilis
HSV Chalmydia
o Common. Neonatal infection rare but serious o 5% pregnancies.
o If primary infection <6wk before delivery high RISK and C o Neonatal conjunctivitis and pre-term labour
section delivery o Azithromycin
o Rx: aciclovir
Parvovirus Bacterial vaginosis
o 0.25%, increasing with epidemics o COMMON. Association with pre term labour
o Fetal anaemia and hydrops (inutero transfusion_ o Treatment: metronidazole
o IgM +ve
o Surveillance with USS and MCA Doppler

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UTI in pregnancy Liver disease in pregnancy

 Common
 Association with pre-term labour & anaemia
 20% leads to pyelonephritis (fever, rigor, tender flank and
abdominal pain, tachycardia, dysuria)
 Treatment: Amoxicillin
VTE in pregnancy
 Pro-thrombotic state; greatest postnatally
 Due to increased. clotting factors and reduced fibrinolytic
activity
 Reduced BF due to mechanical obstruction or immobility.
 Hyperemesis Gravidarum causes dehydration, which
increases risk. Inflammatory conditions do as well
 Risk factors: BMI >40 with GD or pre-eclampsia; CS;
increased hospital stay; other medical illness; IV drug user;
thrombophilia; subfertility and miscarriages
Acute fatty liver (1 in 9000)
 Acute failure, DIC and decreased BG (associated with pre-
eclampsia)
 Presentation: malaise, vomiting, jaundice and vague
abdominal pain. Thirsty ++ for weeks before
 Early Dx and prompt delivery
 Supportive treatment: Dextrose and blood products +/-
dialysis
Intrahepatic cholestasis of pregnancy (0.7% and 50%
recurrence)
 ITCH with no rash, yet abnormal LFTs (raised ALT & AST)
 With any itch: need to exclude!!
 Abnormal sensitivity to cholestatic effect of oestrogen
 Increased risk of still birth & pre-term delivery (toxic bile
salts precipitate fetal arrhythmias)

 PE is the most common cause of maternal death. Presents
with SOB, pleuritic chest pain, haemoptysis cold,
lightheadedness, pins and needles, N&V
 PE investigations: ABG & CXR or V/Q scan vs CTPA. NO D-
dimer as already raised in pregnancy.
 Investigations: CTG, FBP, U+E, LFTS, bile acids
 Management: UDCA relieves itch or PIRITON. Increased
risk of haemorrhage: give vitamin K 10mg OD from 36wk.
Advice to avoid perfume and body lotions.
 IOL at 38wk. 6 week follow up.

 DVT is more common; L iliofemoral vein. Doppler diagnosis Abdominal pain in pregnancy: DDx
 Signs: swelling (difference in calf circumference), deep calf
tenderness, redness and increased temp o Miscarriage/ ectopic pregnancy
o Pre-eclampsia (RUQ)
Management: o Pre-term labour contractions
 Clexane 1mg/kg BD. Doesn’t cross placenta and isn’t o Placental abruption
associated with increased bleeding peri-partum and low o Gall stones (progesterone dilates SM in gall bladder
thrombocytopenia risk. Stop during labour if possible and and bile duct; risk of gall stone pancreatitis)
restart 24 hours later. o Renal colic
 IOL planned for 38/39wk. Reduce dose day before – if not o Chorioamnionitis (Rx with amoxicillin, clarithromycin
reduced, can’t use epidural (Entanox and remifentanyl) +/- gentamicin)
 Continue postnatally, no warfarin in breastfeeding
 Prevention: mobilize and maintain hydration; compression
stockings; antenatal prophylactic LMWH +/- postpartum
 Enoxaparin 40mg OD in every future pregnancy and Hyperemesis gravidarum
continued for 6 weeks postpartum.  Severe nausea and vomiting in pregnancy (NVP) with
 Oestrogen preps contraindicated, encourage weight loss weight loss, dehydration and electrolyte abnormalities
and there is a higher early pregnancy loss.  Usually settles at 14wk
 Exclude UTI, multiple or molar pregnancy

Management:
o Admit if ketosis
o 3L 09% saline and 20mmol KCl
o 1L 0.9% with 10ml Pabrinex (prevent Wernickes)
o Measure weight, HR, postural BP
o Bloods: FBC, U+E, LFTs, TFTs
o Urinalysis and MSU (rule out UTI)
o USS (rule out molar pregnancy)
o Anti-emetics (cyclizine) and steroids if severe

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Antepartum Haemmorhage (>20 wks)  Maternal risk: PPH, postpartum sepsis or placenta
 In 2 – 5% pregnancies accreta
 Usually small, but can indicate future complications  Fetal risk: preterm birth, growth restriction, fetal
 DON’T DO VE UNTIL USS congenital malformation
 History: trauma or sex, amount, colour, clots, mucous, onset,
pain, contractions, previous episodes Presentation:
 Examination: basic observations, fluid status, abdomen for  *PAINLESS BLEEDING*; increasing frequency and
tenderness, contractions, lie, speculum to assess bleed and intensity over weeks with normal fetal movements
cervix, USS before VE - movements and CTG** and fetal HR
 Examination: Breech presentation & transverse lie, no
Management: fetal head engagement
o 2 large bore cannulas  DON’T DO VE AS CAN PROVOKE BLEED
o FBC, G+Cx, U+E, coag screen, Kleihauer (anti-D)
o IV fluids, colloid +/- transfusion, anti D
o USS
o **NO TOCOYLYTICS AS INCREASED DVT RISK**

1) Placenta praevia (0.4%) – unknown cause

 Placenta in lower segment; remember normally low lying @
20wk then migrates upwards…
 10% PP also have placental abruption.

 Placenta implants in myometrium, involving internal cervical

os
o MAJOR; in lower segment yet not involving os
o MARGINAL
- Grade I  placenta in lower seg, doesn’t reach Cx os
- Grade II  lowed edge of placenta reaches but doesn’t
cover the internal Cx os
- Grade III  placenta partially covers the os
- Grade IV  placental covers the internal os

 Risk factors:
o High parity
o Older women
o Multiple pregnany
o Scarred uterus – Hx C section or IVF or multiple
EVACs
o Smoking and cocaine
o Hx placenta praevia

 Complications:
o Obstructs engagement of head therefore transverse
lie & C section
o Severe haemorrhage
o Implant on previous scar which may prevent
placental separation (ACCRETA)
o Penetrate onto uterine wall (INCRETA)
o Surrounding structures (PERCRETA); risk of subsequent hysterectomy

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2) Placental abruption (1%) 3) Vasa praevia (1 in 4000)

 Many APH of ‘undetermined origin’  Fetal BV runs in membranes overlying presenting part.
 Revealed or concealed  UC attached to membranes then placenta (Velamentous
 Degree of PV bleed doesn’t reflect severity – clinical signs key insertion)
 Risk factors:  Painless moderate bleed @ amniotomy or SROM.
o IUGR M t C ti ithi 5 in
o Maternal smoking
o Pre-eclampsia or HT
o Previous abruption
o Trauma
o Multiple pregnancy
o High parity
o Rheumatoid arthritis
o Placenta praevia

Presentation:
 PAINFUL BLEED (constant with exacerbations), of DARK RED blood. REDUCED MOVEMENT and CTG abnormalities.
 Examination: Tachycardic, pallor, hypotension. Tender WOODEN uterus with contractions – UTERUS COUVELAIRE. Abnormal/
absent fetal heart. Coagulopathy and poor UO and renal failure if severe.
 Investigations: Clinical Dx. CTG. USS excludes praevia. FBC, coag and G+Cx +/- catheterization with hourly UO. Regular bloods
as above (with U+E and CVP)

Management:
 ABCDE
 Admission
 IV fluids +/- transfusion
 Steroids for <34wk
 Opiate analgesia
 Anti-D if Rh-ve
 If fetal distress urgent CS.
 If no distress and gestation >37wk IOL with ARM.

Postpartum Haemmorhage RBC iso-immunization

Primary PPH  Rhesus genotype has 3 gene pairs: Cc, Dd, Ee.
 Loss >500ml <24hours  dd = Rh-ve; recognize D antigen of fetal blood as foreign
 RF: Previous Hx or CS; instrumental; retained placenta; APH; therefore express anti-D Ab in response.
anti-coag Rx; overdistension  polyhydramnios, multiple  Secondary exposure in next pregnancy – exponential increase in
pregnancy, high parity, uterine malformation or fibroids, Ab production – cross placenta & binds – Rhesus haemolytic
prolonged or IOL disease
Sensitizing events:
4T’s o Termination of pregnancy/ ERPC
 TONE: atonic uterus – laxity due to overdistension, multi o Ectopic pregnancy or vaginal bleed <12wk
 TRAUMA: Perineal or high vaginal tear/ episiotomy o ECV
 TISSUE: Retained placenta o Amniocentesis or CVS
 THROMBIN: coagulopathy – congenital disorders/ anti-coag Rx/ DIC o Intrauterine death
o Delivery
 Examination: WOODY uterus +/- pain +/- blood loss
 Increased HR, N&V, faint, prolonged CRT, BP doesn’t fall until  Give 1500U anti-D <72hrs after sensitizing events
1.2L+ loss.  All Rh-ve @ 28wk receive anti-D after screening.
 Prevention: IM syntometrine in 3rd stage  KLEIHAUER TEST: number of fetal RBC in maternal circulation –
detects fetomaternal haemorrhages (may need increased dose)
Management:
(1) ABCDE with high flow O2 and 2 large bore cannulae. FBC, coag Manifestation of Rh disease:
and G+Cx for 6 units. o Neonatal jaundice and anaemia. If severe, in utero

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CHECK U&E, LFTs (HELLP syndrome screen) anaemia (hydrops fetalis – cardiac failure, ascites and
(2) Give fluids, transfusion of blood and FFP oedema)
(3) Manual fundal compression +/- medications: o Doppler USS of peak velocity in systole (PVS) of fetal MCA
- 40U of syntocinin in 500ml of 0.9% Normal saline over 4 – high sensitivity for anaemia <36wk; use every 2wk in
hours (SE: hypoNa) high risk pregnancies.
- 500μg Ergometrine IV (SE: Faint, increased BP, chest o Rx: in utero transfusion.
tightness, cramps)
- 250μg carboprost IM every 15min to max 2mg (8)
HYDRATIFORM MOLES
 Gestational trophoblastic disease
- 800μg Misoprostol PR
 Extremities of age and Asians
(4) Head down tilt (short term to improve VR but may compromise
ventilation) and catheterization
(1) Local and non-invasive = HYDATIFORM MOLE
(5) Bimanual compression if no improvement with meds
o COMPLETE: parental, sperm fertilizes empty oocyte, mitosis
(6) Rusch balloon, B lynch brace suture, uterine artery ligation, iliac
diploid 46 XX. Generalized swelling of villous tissue – no fetal
artery embolization tissue. Diffuse trophoblastic hyperplasia
(7) Hysterectomy SNOWSTORM appearance with large uterus.
15% become invasive.
o PARTIAL: 2 sperm and oocyte, triploid. Focal swelling of focal
Secondary PPH trophoblastic tissue. Evidence of fetus. 0.05% become invasive.
 Excessive blood loss >24hrs to 6wks
 Endometritis +/- retained tissue (2) Malignant and invasive = Gestational trophoblastic
 Examination: Enlarged uterus and tender with open internal neoplasia (persistent high HCG)
cervical os o Metastatic choriocarcinoma (both are more likely after
complete molar pregnancy)
**Need to remove and follow up BhCG
Management:
 History of bleeding and vomiting
(1) Vaginal swabs and FBC +/- G+Cx if severe.
 Examination: large uterus, early pre-eclampsia and
(2) Antibiotics.
hyperthyroid
(3) ERPC. More chronic bleed with endometriosis therefore
 Investigation: USS. SNOW STORM (Complete moles)
prolonged antibiotics.
Management:
(4) Histology ?gestational trophoblastic disease.
 Remove by EVAC, repeat serial hCG. Chemotherapy for GTN
 DO NOT get pregnant or use pills until normal hCG. Can
increase need for chemo
 RECURRENCE: 1/60 pregnancies (constantly monitor HCG)

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MISCARRIAGE
Complete miscarriage Positive pregnancy test weeks ago.
EDD: LMP - 3 MONTHS + 7 DAYS + 1 YEAR Heavy fresh vaginal bleed and
abdominal cramps, passed in
 As long as several clots. Pain stopped and
the cycle is regular 28 days, ovulation on 14th day minimal bleeding. Uterus normal
 Crown rump length (CRL): 9-14wks pre-pregnancy size and cervical os
 Head circumference (HC): 14-20wks closed
Incomplete miscarriage Positive pregnancy test weeks ago.
SYMPTOMS OF PREGNANCY & HISTORY TAKING Cervical os remains open, only
 Normal symptoms of pregnancy some POC have been passed. Need
 Hx: EDD, USS, plans and concerns, problems so far including to remove from os with sponge
holding forceps.
bleeding, pain, contractions or fluid loss
Septic miscarriage Positive pregnancy test weeks ago.
 PMHx gynae: PID or PCOS (longer cycle and GD risk)
Tissue from above has become
 OHx and contraceptive (coil and miscarriage risk) infected and risk of septicemia.
 Last smear and result Tender +/- fever. Cervical os
 Surgical Hx remains open.
 FHx of cardiac problems, VTE, pre-eclampsia, DM, twins, Threatened miscarriage Bleeding during the pregnancy,
autoimmune or congenital problems prior to viability that has yet to be
 Investigations: assessed further. Foetus still alive,
o FBC for anaemia os close and uterus of expected
o Blood group and antibodies size (25% RISK)
o Urinalysis Missed miscarriage Brown bleeding, uterus small and
o Rubella (dangerous in 1st trim – vaccine after preganancy) cervical os remains closed.
o HepBsAg (transmit in labour and vaccine needed at birth)
Recurrent miscarriage 3+ miscarriages in succession.
o HIV (anti-retroviral, CS and no breast feeding to reduce risk of
Chance in 4th pregnancy is 40%.
transmission 30 to <1%)
Increased risk with age.
SCREENING:
Check APL antibodies (thrombosis
 Down’s syndrome  11 – 13wk: NT and PAPP-A and hCG; in utero-placental circulation. Give
combined with mothers age and gestation of baby to give aspirin and low dose clexane)
result. Triple test: HCG, AFP, uE3 (+ inhibin for quadruple) Investigations for recurrent miscarriage:
and structural anomaly scan at 20wk.
 Gestational diabetes  OGTT at 24-28wk if risk with BMI
>30, previous baby >4.5kg, previous GD, 1st degree relative
T1DM, origin
 Pre-eclampsia  screen at every visit (BP and urinalysis)

EARLY PREGNANCY PROBLEMS

 Investigations: TVUS, hCG testing and symptoms
 If no sac on TVUS, look for free fluid in POD for early, ectopic or
early complications.
 Zygote enters uterus at day 4 in morula stage
 Morula  blastocyst (fluid cavity within); trophoblast  placenta
(complete by week 12)
 Trophoblast produces hCG (peak at 12wk) which maintains corpus
luteum
 Implantation days 6-12
 HR by week 4 or 5; USS 1 week Risklater.
factors for miscarriage:
o Age
 Previous
1 in 5 pregnancies with 50% overo40 year olds miscarriage or
 multiple pregnancy.
70% miscarriages due to abnormal karyotypes of POC. 2/3 are
o Environmental exposure
autosomal trisomies; most in 1st trimester.
to tobacco smoke, drug
 Wait 2-3 normal cycles, allows body to return to normal and
or alcohol use
recover o Medial: Diabetes or SLE
ECTOPIC PREGNANCYo Obesity
Management of ectopic pregnancy:
 ABCDE
 Commonly in fallopian tube (85%)  Intially NBM and IV access
 Ampulla (55%), isthmus (25%) and fimbrae (17%)  Bloods: FBC, G+Cx
 Ix: BhCG and USS
 Medical, conservative or surgical management

(1) Conservative
22 o Small and not ruptured
o BhCG low <1000 and decreasing ++
(2) Medical
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 TRIAD of symptoms:
o Lower abdominal pain (colic then constant)
o Dark bleeding following amenorrhoaea
o Collapse in 20%. Some syncopal episodes

 Consider if persistent pain and vaginal bleed.

 Also shoulder tip pain if rupture then collapse, pain on defecation.
 Risk of hypo-volaemic shock
 Signs: tachycardia, hypotension, cervical excitation and tender adnexae. Closed os and uterus smaller than expected.

 Investigations:
PIPPA: Risk factors for ectopic:
o BhCG: (urinaryectopic
o Previous and serum) on all females with lower abdominal pain
<1000
o IUD repeat in coil
(copper 48hours, 63% rise is normal. Slow rising or decreased is indicative
only stops
o TVUS:IUno intrauterine sac and free fluid in adnexa +/- sac within.
pregnancies)
o PID
Multiple pregnancy Molar pregnancy
o Pelvic or tubal surgery
Hyperemesis gravidarum Prolonged hyperemesis
Recurrent PV bleed/ staining
Hyperthyroid 3%
Early pre-eclampsia

Firm, normal uterus Soft, doughy uterus

Vesicles on vagina
hCG >100,000

Two sacs with two fetus on USS Snowstorm apperance

Cystic placenta
Ovarian theca lutein cysts (20%)

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MULTIPLE PREGANCY(1 in 80) TTTS (Twin to twin transfusion syndrome)

 Associations: IVF, age, high parity, maternal FHx, black race  15% monochrorionic pregnancies with vascular
 Larger uterus also with wrong dates, hydratiform mole, fibroid, anastomoses in the placenta.
ovarian cyst and full bladder – not necessarily twins  Arterioarterial and venvenous anastomoses are
superficial, allowing flow in both directions.
(1) Dizygotic twins (70%)  2 eggs, non-identical Arteriovenous anastomses are deep, unidirectional flow
o Dichorionic diamniotic twins (DCDA) – lambda sign (thick (skipping 1 twin’s artery).
V shaped echogenic area at the placental edge of  Bidirectional AAA protective in balancing this out.
membranes)  Donor twin (anaemic, hypovolaemic, oliguria,
o Hereditary – maternal FHx of twins/ paternal no oligohydramnios and growth restriction)
revelence  Recipient twin (polycythaemia, hypervolaemia, polyuria,
(2) Monozygotic twins (30)  1 egg, then divides; identical hydrops)
o Depending on how long after fertilization the splitting  Management: USS 2weekly from 16-24wk. Treatment
occurs: with fetoscopic laser ablation
o Day 0-3/4: 30% cases – DCDA
o Day 4-8/9: 70% cases – MCDA (T sign)
o Day 9-12: <1% cases – MCMA
o Day 12+: Conjoined twins (RARE)

Fetal risks Maternal risks

Perinatal moratily increases x10
(asphysia x5)
Stillbirth
Prematurity
IUGR
Major congentital abnormality 5%
(higher in mono) CP risk x8
Cord accident – malposition,
malpresentation, PROM or
preterm
Operative delivery – birth trauma;
lower APGAR scores (especially 2nd
twin)
Increased symptoms of early
pregnnancy (esp HG in 1st trim)
Increased risk of miscarriage/
vanishing twin syndrome
ANAEMIA (more haemodilution)
Minor disorders – backache,
pressure problems, SOB or UTI
APH from atonic uterus and
greater risk of PPH
HTN, pre-eclampsia
Polyhydraminos

 Need consultant led, hospital based care – close surveillance (2

weekly from 20wk)
 Management anterpartum: Early detection of PIH, serial
growth scans from 24wk, prophylactic IRON & FOLIC ACID (2nd
trim), counselling with risk and early signs of preterm labour.
US each separately for growth, fluid, placenta & movements

DCDA delivery at 36-38wks

- Vertex:vertex presentation – vaginal birth
- Vertex:non-vertex presentation – requiers specific
manoeuvres for 2nd twin – ECV or internal podalic
version; section for 2nd
- 1st twin non-vertex – C section

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BREAST FEEDING General advice:

Protective features:
 Reduced risk to baby of GASTROENTERITIS*, RTI, OM, UTI,
atopic disease, NEC, diabetes, RF for CVD
 Protective to mother against breast/ovarian Ca, hip fractures
Development:
 Development of ductal system and alveoli by O, P and hPL
 Acini cells in alveoli produce milk and myoepithelial expel.
 Montgomery tubercles produce lubricating fluid.
 After the placenta is deliver, O and P decreases and prolactin
increases.
 Levels of prolactin peak after 1st feed increasing milk
production. Stimulation of nipple essential– prolactin receptor
cells need primed early to prevent shut down and decreased
milk production potential. Also stimulates mothering.
 Oxytocin produced in posterior pituitary gland. Causes myo-
epithelial cells to contract, ejecting milk. Stimulated by seeing,
touching or smelling the baby. Induces maternal well-being.
 Feedback inhibitor of lactation (FIL) inhibits secretion. If the
breast is full of milk, FIL slows down further production/vv.
Mother has to expel milk if not breast feeding.
 SKIN contact & early 1st feed (within 1 hour) to keep baby
warm, regulate HR and RR
 Encourages bonding
 Stimulates hormonal response and facilitates breast-feeding
 Good positioning & effective attachment with baby-led feed
 Avoid supplements (dampen appetite), teats or dummies (alter
how baby sucks).
 Infrequent feeding: delayed 1st feed; lack of demand feeding;
supplements; separation; teats
 Poor attachment: pain and damage to nipple; sore and cracked
nipples; engorgement (day 1-5 with breast feeling swollen,
lumpy and full) or stasis (risk of mastitis in one breast); poor
milk supply; baby unsatisfied and frustrated with failure to gain
weight
 Good signs: long slow sucks with pauses, cheeks will round
and full and lips are wide; drawing sensation to breast; baby
alert and relaxed, ending the feed; undistorted

COLOSTRUM
o Laxative effect encouraging meconium passage,
minimizing jaundice
o High density and low volume – rich in PROTEN, FAT
SOLUBLE VITAMINS (A,E,K) and other minerals than
mature milk
o Less lactose, fat and water soluble than mature milk
o Ig  against past maternal infections, SIgA protecting
against pathogens sticking to mucosa, GALT and BALT
protect from environment (Peyer’s patches in maternal
gut)
o Lactoferrin  binds free iron in baby’s gut increasing
absorption and iron-dependent bacteria (E coli) can’t
grow, allowing normal flora to thrive
o Bifudus Factor  help lactobacillus bifidus create acidic
pH in gut killing pathogens
o Hormones  insulin, TSH, GH, EGF & enzymes  lipase
o WCC and viral fragments to digest bacteria & trigger
immune response

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GYNAECOLOGY

 GnRH is released by the hypothalamus in pulses (changes in

amplitude and frequency)
 FSH and LH, TSH, prolactin and hCG is released by the anterior
pituitary. All have alpha subunit, hence why BhCG is measured in
pregnancy test

 1000 follicles develop in each ovary; one ovulated to become the

dominant follicle (Graafian follicle)
 Pulses of GnRH; increasing LH and FSH
 Production of oestrogen and inhibin; negative feeback on FSH so
that only one follicle matures; with positive feedback on LH.

 LH surge at day 14; ovulation occurs within 36 hours (naturally a

raised LH in PCOS, be aware of false +ve)
 Increase in oestrogen: proliferation of stromal cells and
elongation of gland
 Becomes the corpeus luteum hence increasing levels of
progesterone. Peak of levels at day 21.
 Corpeus luteum is yellow and rich in fat
 Surrounded by granulosa cells, which become increasingly vascularized in the luteal phase (avascular in follicular phase)

 With failure of fertilization, falling oestrogen and progesterone

 Rhythmical vasoconstriction and dilation of spinal arteries causing stasis and ischaemia of endometrium
 Red blood cells leak in the stroma causing an interstitial haemorrhage, leading to further ischaemia
 Binding membrane of the endometrium is breached and blood is released into the uterus
 Separation of the spongiosum and basilis layer – endometrial regeneration

MENORRHAGIA IRREGULAR MENSTRUATION & IMB

 Excessive bleeding >80ml  With or without menorrhagia
 Anovulatory cycles COMMON: physiological after menarche
AETIOLOGY: and peri-menopause
o Dysfunctional uterine bleeding (80%): subtle
abnormalities in endometrial fibrinolytic system and uterine AETIOLOGY:
prostaglandin levels o Fibroids (with HMB)
o Uterine fibroids (30%) & polyps (10%) o Uterine/ cervical polyps
o Endometriosis o Endometriosis (with pelvic pain)
o Chronic pelvic infection o Adenomyosis
o Ovarian/ endometrial/ cervical Ca o Ovarian cysts
o RARE: VMB disease, anticoagulation treatment, o Chronic pelvic infection
thyroid disease o Atrophic vaginitis (if post-menopausal)
o Carcinoma
 HISTORY: amount & timing; flooding & clots; contraception;
last cervical smear; anaemic features and fitness levels; Investigations:
tenderness or distension; pressure symptoms; infective signs o FBC and coag screen
o TFTs
Investigations: o TVUS for endometrial thickness or masses. Do
o FBC and coag screen endometrial Bx with pipelle
o TFTs o Chlamydia swab
o TVUS for endometrial thickness (>3cm – o Speculum exam

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hysteroscopy)
o Chlamydia swab Management:
 RED FLAG: IMB >3 cycles/ 40+ (PMB) (1) Mirena coil or COCP: gives regular and lighter menstruation.
HRT can be considered in peri-menopausal
Management: (2) Avulsion of polyps and send for histology
(1) IUS (Mirena coil: reduces BF 90% and acts as
contraception. The copper coil actually increases loss)
(2) Tranexamic acid 1g TDS (during menstruation only and
reduces blood loss by 50%) & Mefenamic acid 500mg When to do a hysteroscopy?
TDS (with pain: inhibits prostaglandin synthesis –
reduces blood loss 30%) or COCP o Thickness >10mm or patient >40yrs
o Better than mini pill as less effect on bleeding o ?polyp on USS +/- IMB
loss o No response to treatment
(3) GnRH analogue with or without HRT
o Limited to 6/12 as risk of osteopenia
(4) Endometrial laser ablation or diathermy rollerball
endometrial ablation, TCRE – risk of uterine perforation
and decreased fertility
(5) Thermal balloon ablation, circulate hot saline,
cyrotherapy
(6) TCRF: submucosa fibroids: <3cm – improve fertility
(7) Hysterectomy
(8) UAE
AMENNORHOEA & OLIGOMENORRHOEA POST COITAL BLEEDING (PCB)
 Primary: Periods didn’t start by 16 otherwise normal sex AETIOLOGY:
characteristics or no secondary sex characteristics by age 14 o Atrophic vaginitis (post menopause)
Delayed puberty or menstrual outflow obstruction? o Cervical ectropion (young F on OCP at menstruation/
pregnancy)
 Secondary: Previous normal & ceased for 6+ months o Cervical polyps
o Cervicitis
AETIOLOGY: o Cervical Ca
o Physiological
Pregnancy; post menopause; lactation; familial; Management:
constitutional delay  Inspection & smear for cytology
 Avulse polyp & send for histology
o Hypothalamus: Hypothalamic hypogonadism  Freeze ectropion with cryotherapy
Hypothalamus effectively shuts down  Colposcopy to exclude malignancy
Associated with Low BMI and excessive exercise/stress
Low GnRH, LH and FSH, oestrogen
Supportive Rx & oestrogen replacement through COCP
or HRT as risk of osteopenia

Pituitary: Hyperprolactinaemia
o
Adenoma or hyperplasia
DYSMENNORHOEA
Low GnRH, FSH and LH, oestrogen and high prolactin
 Primary: no organic cause
Rx: Bromocriptine or Cabergoline
 Management: Mefanemic acid or COCP and reassurance
Rare: Sheenans syndrome after PPH causes pituitary
necrosis & hypopituitarism
 Secondary: pelvic pathology; pain precedes and is relieved
o Adrenal or thyroid
at onset of menstruation; deep dyspareunia; menorrhagia;
Over or underactivitity
IMB
Hypothyroid – Increased prolactin & amenorrhoea.
Congenital adrenal hyperplasia rare
 AETIOLOGY:
o Fibroids
o Ovary

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PCOS with amen or oligomenorrhoea +/- subfertility o Adenomyosis: tenderness and irregular enlargement
Premature menopause o Endometriosis: tenderness, immobile
High LH, low oestrogen. Free androgens >5 o PID
Turners syndrome (45XO – short stature and poor 2 sex o Ovarian cysts/ tumours
characteristics; normal intellect)
Gonadal agenesis  Investigations: Pelvic USS and laparoscopy
Androgen insensitivity  Management:
o Removal of mass
o Outflow obstruction problems o Adhesiolysis
High GnRH, FSH and LH, oestrogen o Remove cysts >5cm
Imperforate hymen
Transverse vaginal septum: risk of haematometra
Rokitanskys syndrome or mullerian agenesis: absence or
undeveloped uterus and vaginal; varying degrees of
vaginal hypoplasia; external genital normal.

o Ashermanns syndrome (uncommon)

Excessive D&C/ ERPC

o Cervical stenosis secondary to haematometra

CERVICAL ABNORMALITIES
ACUTE CERVICITIS
 Endocervix: columnar glandular; ectocervix: squamous.  STI: CT or NG most common
 Meet @ squamocolumnar junction. Vulnerable to neoplastic  Ulceration & infection with degrees of prolapse
change, as it meets lower pH of vagina.  Management: Antibiotics depending on culture
 Partial eversion physiological in puberty/ pregnancy.
CHRONIC CERVICITS
CERVICAL ECTROPION  Chronic inflammation or infection often of an ectropion.
 Visible columnar epithelium as ‘red area’ around cervical os,  PV discharge
due to eversion. Normal in younger; pregnancy; OCP.  Management: Cryotherapy +/- antibiotics
 Assymptomatic; sometimes discharge or PCB or dyspareunia
 Management: Smear to exclude Ca. Cryotherapy. Exposed NABOTHIAN FOLLICLES
area is susceptible to infection  Squamous epithelium formed over endocervical cells
 Secretions from the underlying glandular cells are blocked
CERVICAL POLYPS and retained forming a cyst
 Benign tumours of endocervical epithelium.  Opaque white swelling.
 Common 40+ and <1cm  Treatment not needed unless symptomatic
 Assymptomatic; IMB/PCB
 Management: Avulsion & sent for histology. LA

CERVICAL INTRAEPITHELIAL NEOPLASM CERVICAL CARCINOMA

 Atypical cells amidst squamous cells.
 Associated with HPV 16 +18
 UK vaccination programme. Screening from age 25
 High false positives if before as physiological
abnormalities
 Cusco’s speculum to scrape loose cells @ transformation
zone – sent for Liquid based cytology (LBC)
 Dyskaryotic (large nuclei with frequent mitoses of
increasing size) suggesting presence of CIN.
o CIN I: mild atypia of lower 1/3
o CIN II: moderate atypia of lower 2/3
 Peak @ 30 & 80. Majority 24-49.
 90% squamous cell carcinoma; 10% adenocarcinoma with
worse prognosis
 Presentation: PCB, offensive vaginal discharge, IMB or PMB,
no pain (later stages spread to rectum or bladder with PR or
haematuria or pressure symptoms)
 Diagnosis: Bx or visible mass; ulcerative lesion or EUA +/-
MRI for size, spread and lymph node involvement.
 Staging via FIGO

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o CIN III: severe atypia full thickness of epithelium – o Stage 1 lesions are confined to cervix
carcinoma in situ – no invasion. o Stage 2 invasion into vagina, but not the pelvic side
 90% patients <45; peak prevalence 25-29 wall
 RISK FACTORS: OCP, smoking & immunocompromised. o Stage 3 invasion into lower vagina or pelvic wall, or
Poor diet, ++ partners, HIV, steroids. causing ureteric obstruction
 Screening: o Stage 4 invasion of bladder or rectal mucosa, or
o Normal: repeat in 3 years 25-49 or 5 years 50-65 beyond true pelvis.
o Borderline and HPV –ve: Routine recall  Treatment:
o Borderline and HPV +ve: Colposcopy referral o Stage 1a(i): Cone Bx or simple hysterectomy
o Moderate to severe dyskaryosis – Urgent o Stage 1a(ii) to 1b: Laparascopic
colposcopy lymphadenectomy & radical trachelectomy
o Look up referral guidelines…** o Stage 1a(ii) – 2a: Radical abdominal/
 Prevention: HPV vaccine; sex and contraceptive Wertheims hysterectomy or chemo-
education; cervical smear programme radiotherapy
 Treatment: CIN II-III – LLETZ in OP o Stage 2b+: Chemo-radiotherapy alone
(palliation)

LICHEN SCLEROSIS LICHEN PLANUS (the Ps)

 Autoimmune, linked with alopecia, thyroid disease and vitiligo.  Autoimmune. Similar to lichen sclerosis however includes
50+ skin or mucousal surfaces – genitals, wrists

 Examination: Vulval pallor, fusiolabia, featureless vulva with  Presentation: Pain++, pruritis, purple papules or plagues
skin tightening, telangiectasia in late disease. In the anogenital on vulva with white hyperpigmentation
area: figure of 8 distribution  WICKHAMS striae
 Presentation: Pruritis, sore and dyspareunia. Pruritis typically  Management: topical steroid
worse at night
 Management: topical steroid BD until symptoms resolve. Scabies have silver burrow lines. Pediculosus are nits.
Weekly maintenance
 Complications: 5% develop vulval carcinoma. Association with
VIN

VULVODYNIA/ VULVAR DYSAESTHESIA VIN

 Usual type VIN
o Mostly all VIN: warty, basaloid, mixed
 Diagnosis of exclusion; some associated with STI or COCP or
o Can develop SCC
psychosexual histories
o 35-55
 Essential or spontaneous generalized: Burning pain in older
o Associated with HPBV16, CIN, smoking, chronic
women
immune diseases
 Vestibular: more superficial dyspareunia and pain with
o Multi-focal and varied appearances: red, white or
tampons
pigmented plaques, papules or patches; erosions;
nodules; warty or hyperkeratosis
o Presentation: pruritis, pain
o Treatment: emollients and topical steroid; surgical
excision
 Differentiated VIN
o Rarer
o Association with lichen sclerosis, hence occurs in
older women
o Unilocal and ulcer/plaque
o Some develop KSCC

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o Higher risk of progression to cancer than usual type

BARTHOLINS CYST VULVAR CARCINOMA

 Bartholinitis: medial to labia minora  95% SCC

 Gland becomes blocked and inflamed. Abscess forms if the  other: melanoma or BCC
cyst becomes infected (staph or e coli)  5% genital tract cancers
 Physical blockage with mucous or inflammation  50% present stage 1. Stage 1a wide local excision
 NOT AN STI  Others may need groin lymphadenectomy through skin
 Associated with smokers sparing incision (Triple incision radial vulvectomy)
 Presentation: Assymptomatic therefore no treatment needed.
Some have superficial dyspareunia or pain on sitting.
 Treatment if symptomatic: Marsupialization – incision sutured
open to reduce risk of re-formation

UTERINE AND VAGINAL PROLAPSE URINARY INCONTINENCE

 Most parous F; 10-20% seek medical attention.
 Voiding is dependent on the detrusor contractility and
TYPES: coordinated urethral relaxation.
o URETHROCELE: Lower  Maximum store 500ml; first urge @ 200ml.
anterior vaginal wall  Distension of bladder wall causes afferent fibres to signal to
o CYSTOCOELE: Upper SC.
anterior vaginal wall  Efferent parasympathetic cholinergic nerves innervate the
(involving bladder +/-
detrusor smooth muscles causing a contraction once
urethra for cysto-
urethrocoele)
threshold is reached.
o APICAL/ VAULT  Simultaneous relaxation of the smooth muscle at the bladder
PROLAPSE: Uterus, cervix & upper vagina – grading in relation to neck and external striated muscles by sympathetic response.
hymen at introtius  Micturition reflex controlled at Pons; modified within
o ENTEROCOELE: Upper posterior vaginal wall including Pouch of cortex to relax.
Douglas
o RECTOCOELE: Lower posterior vaginal wall (including anterior wall of TYPES OF URINARY INCONTINENCE:
rectum)  Urodynamic stress incontinence: USI (cough; sneeze;
exercise):
AETIOLOGY **DIMCHOC**: o Increased intra-abdominal pressure (eg.
o Delivery (Large infants; prolonged 2nd stage; instrumental) Pregnancy) increases pressure on the bladder
o Iatrogenic from surgery o POOR FASCIAL SUPPORT to pelvic floor
o Menopause (atrophy: less oestrogen deteriorates collagen o Childbirth direct damage or neuropathy
build up) o Menopausal atrophy with less collage
o Congenital (collagen abnormality; Ethlers Danlos) o Congenital weakness
o Heavy lifting o Trauma
o Obesity  Over active bladder: OAB (urge, frequency 8+, nocturia,
o Chronic cough or constipation leakage):
o Over activity of the detrusor muscles; determined
 Presentation of prolapse: Dragging sensation or lump, by uro-dynamics
worsens throughout day or standing; interference with sex; o Neurogenic (with MS, SC injury, degenerative
ulceration and bleed or discharge. Pressure symptoms of disease)
urinary frequency or stress incontinence or defecation o Idiopathic
problems. o Poorly controlled diabetes, functional immobility
and chronic pelvic pain worsens symptoms
 Investigations: Pelvic USS, uro-dynamics; fitness for surgery o Exclude infection/?Hx childhood enuresis
with ECG/ CXR/ FBC and U&E  Chronic retention or fistula:
o Obstructed labour association in developing
world
Management:

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(1) Pelvic floor exercises and physio; weight reduction and

stop smoking  Congenital:
(2) Shelf or ring pessary changing at 6 months +/- HRT or o Duplex kidney
topical oestrogen o Extra ureter into bladder or vagina – exclude in
(3) Vaginal hysterectomy (40% vag hyst later present with young presentation
vaginal vault prolapse) or sacrospinous fixation or
sacrocolpopexy (vault) or anterior/posterior repair (vaginal Leakage on coughing not necessarily stress incontinence; may provoke
wall prolapse) OAB; differentiate under urodynamics

Physio prior to urodynamics with 40% cure, 40% improve, 20% fail –
bladder emptying techniques, pelvic floor stimulation and exercises

 Investigations:
o Bimanual with cough
o Post void urinary residual
o Urinalysis (Blood for Ca or calculi; glucose for DM;
nitrates & leucocytes for infection; protein for renal
dysfunction)
o USS for congenital problem; calculi; tumour
o Urodynamics
o Diary of voiding intervals and functional capacity
o Methylene dye test ?fistula
o Neuro exam for S3+4 for saddle anaesthesia: then
MRI

Management of USI (50%):

(1) Weight reduction and stop smoking
Decreased fluid intake of caffeine & more water
Spicy food and fizzy drinks may also trigger
PFMT with physio 3/12
(2) Vaginal pessary if prolapse
(3) Duloxetine SNRI however side effects of nausea; dry
mouth; dizzy; drowsy
(4) TVT or TOT; sling

Management of OAB (35%):

(1) Simple advice as above with physio
(2) Bladder retraining: Timed voiding – biofeedback reduces
frequency of accidents, improving control overtime.
Establishes a schedule to urination.
(3) Anti-muscarinic: OXYBUTYNIN (side effects of dry mouth;
confusion therefore caution in elderly) or B3 agonist:
MIRABEGRON (side effects of tachycardia; palpitations and
HTN hence monitor BP & U+E; if headache stop; stroke risk)
(4) Botulinum toxin injections
(5) Topical oestrogen VAGIFEM improves symptoms of atrophic
vaginitis with itch/ dryness
(6) S3 nerve stimulation

 Acute voiding dysfunction: Catheter & drainage; acutely can

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permanently damage bladder from overdistention, damaging

nerve
 ?Assoc UTI/ neuro disease/ common in post op trauma, drugs,
spinal or epidural, outflow obstruction.

Mixed USI and OAB (10%): treat predominant cause

ENDOMETRIOSIS CHRONIC PELVIC PAIN
 30-45 peak age
 Retroverted uterus  Intermittent or constant pain in lower abdomen for 6+
months
 Oestrogen dependent: regress in menopause and pregnancy.  May present with migrane or lower back pain
 Risk factor: nulliparous  Varies of menstrual cycle ?endometriosis or adenomyosis
 Differential diagnosis:
 Common sites affected: ovaries/behind ovaries; uterosacral IBS or interstitial cystitis or psychological secondary to
ligaments; abdominal wound scars or umbilical area; rarely on depression or sleeping disorders.
vagina, bladder, rectum or lungs
 Appearance on scan: red dot, black powder burn dots, large Management:
raised red or black vesicles. White area of scarring and o COCP
surrounding abnormal blood vessels. Severe disease has o GnRH analogue with add back HRT
extensive adhesions and ovarian endometriomas o IUS
o Further laparoscopic Ix

 AETIOLOGY: Possible theories. Retrograde menstruation;

distant foci by BB; lymphatic or mechanical spread or ?genetic
link
 CHOCOLATE CYST (endometrioma on ovaries): accumulated
altered blood
 Inflammation and progressive fibrosis or adhesions
 Severe disease: frozen pelvis with immobile organs from these
adhesions.

 Presentation: chronic cyclical pelvic pain; dysmennorhoea,

relieved by onset of menstruation; deep dyspareunia;
subfertility; dsychezia during menses. Acute pain with
ruptured choc cyst
 Examination: Tender +/- thickening behind uterus or adnexa;
retroverted & immobile if severe

Management:
o Asymptomatic nil
o Analgesia
o COCP MICROGYNON (not in older F or migraine with
aura or smokers)
o Progestogen CERAZETTE or MICRONOR (side effect:
fluid retention and weight gain)
o GnRH analogue PROSTAP injections: however limited
to 6 months with risk of bone demineralization +/-
addback HRT
o Mirena coil

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o Bipolar diathermy +/- adhesiolysis

o Hysterectomy + BSO then HRT

POST MENOPAUSAL BLEEDING Risk factors:

 Average age 51 o OBESITY and SMOKING (risk x3)
 After 1 year amenorrhea with ovarian follicular ( isk 0)
degeneration, decreased O & FSH
 Premature menopause <40

**PMB: ENDOMETRIAL Ca until proven otherwise**

AETIOLOGY:
o Atrophic vaginitis (60-80%)
o Endometrial hyperplasia (10%) +/- polyps (12%)
 With atypia: complex, 30-40% risk of malignancy – hysteroscopy
 Without atypia: low risk – TVS and Bx. Mirena coil

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o Endometrial cancer (10%)

o Ovarian or cervical cancer
o Cervicitis
o Cervical polyps
o Withdrawal bleeds from HRT (7%)
o Bleeding disorders, heparin or warfarin therapy

 Endometrial cancer is the most common genital tract cancer. 5th most common cancer in NI.
 Common 60+

 Presentation: PMB, IMB or PCB, pelvic mass

 Examination: inspect, speculum and bimanual

TYPES:
 Type 1: Endometrioid adenocarcinoma (90%)  pre-malignant hyperplasia atypia coexists in 40%
 Type 2: Papillary serous adenocarcinoma (10%) and clear cell adenocarcinoma (5%) and mixed (5%)  older women, more
aggressive & not related to oestrogen

 Investigations:
o History
o TVUS >5mm in longitudional plane needs Bx. (If on tamoxifen, TVUS isn’t as reliable therefore all need Bx)
o Bx pipelle and hysteroscopy to confirm diagnosis
o STAGING after hysterectomy: do MRI and CXR for any spread.

INFERTILITY (2) Hypothalamic hypogonadism  decreased GnRH. BMI <19,

ANOVULATION (30%)
o Age decreases genetic quality of eggs, not ovulation.
o Detection:
 Mid luteal phase serum P
 USS follicular tracing
 LH based urine predictor kits
 Cervical mucous pre-ovulation acellular and
‘fern’ on dry slide forming SPINNBARKEIT
 Body temp decreased 0.2 pre ovulation and
increases 0.5 luteal phase – temp chart
recording.
(1) POLYCYSTIC OVARIES SYNDROME
PCO on TVUS
 Multiple (12+) SMALL (2-8mm) follicles in an enlarged
ovary (>10mL volume)
PCOS
 As above with irregular periods (>35 days apart)
 Hirsutism (acne and excess body hair +/- increased
testosterone).
 Increased LH and insulin and free androgens
 Normal FSH. Reversed LH:FSH ratio.
 Free androgen index >5 increasing peripheral insulin
resistance
ROTTERDAM CRITERIA:
(1) String of pearls
(2) Hyper-androgenism (Increased free androgens. HIRSUTISM
– acne and excess body hair +/- increased testosterone)
(3) Oligomenorrhogea >35 days/5 weeks (irregular periods)
(4) Prolactin NORMAL
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stress, diets, athlete – need to gain weight
(3) Hyper-prolactinaemia  Adenoma or hyperplasia.
Bitemporal hemianopia, headache, galactorrhoea,
oligo/amenorrhoea. Treatment: Bromocriptine or cabergoline
(dopamine agonist) to reduce prolactin
(4) Pituitary damage with PPH – SHEEHANS SYNDROME
(infarction)
(5) Luteinized un-ruptured follicle syndrome  follicle
develops but is never released. Unlikely to occur each month.
(6) Premature ovarian failure  ovary fails with decreased
oestradiol and inhibin hence no negative feedback and raised
FSH and LH. FSH >30.
Hot flushes and amenorrhoea. Exogenous hormones of no
use as there are no responding follicles. Need donor eggs
(7) Hypo or hyperthyroidism
(8) Androgen secreting tumours
Side effects of ovulation induction
 Multiple pregnancies with clomifene or gonadotrophins
 Ovarian hyper stimulation syndrome (OHSS)
 Risk of hypovolaemia, electrolyte disturbances, ascites,
thromboembolism and pulmonary oedema
 Ovarian and breast cancer
 Monitor with USS or use lower doses. Can ‘coast’ or cancel IVF
cycle by withholding injection if too excessive and treat
complications before resuming.
34
TUBAL DISEASE (20%)
*CHLAMYDIA is a most common cause – subsequent PID*
 Salpingitis, tubal surgical adhesions, endometriosis or
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Management:
o Diet and exercise
o COCP: regulates periods, need 3-4 per year to protect endometrium
o Antiandrogens for hirsutism (cyproterone acetate). Eflomithine for facial hirsutism
o Metformin as 50% devlop DM, 30% GD
o Ovulation induction with:
(1) CLOMIFENE (increasing FSH and LH, blocking oestrogen receptor) at day 2-6 for only 6 months with METFORMIN
if resistant & to reduce early miscarriage risk
(2) Gonadotrophins: FSH injections and monitor oestrogen levels.
(3) Laparoscopic ovarian diathermy with caution of tubal patency, test with methylene blue insufflation
(4) IVF
 Complications: T2DM, GD, Endometrial cancer

 Semen analysis: count >15mil, mobility >40%, normal forms >4%  (4)taken
LAPROSCOPIC
2 days afterOVARIAN DIATHERMY
ejactulation, analysed within 1 hour and
repeated in 12wks.  As effective as gonadtrophics
 Management: General lifestyle advice and drug exposures. Loose clothing  Lower multiple
and cooling. pregnancy
Ligation rates were appropriate.
of variocele
Assisted conception with IUI or IVF and ICSI or donar insemination  Each ovary monopolar diathermy at a few points for
few seconds
 Also assess tubal patency with methylene blune
UNKNOWN CAUSE (25%) insufflation and assess any co-morbidities
 IMPLANTATION OF EMBRYO?
(5) GONADOTROPHINS
 Useful in hypothalamic hypogonadism if weight is
DISORDERS OF FERTILIZATION (30%) normal
 Fimbrial end of fallopian tube collects oocyte from the ovary. Peristaltic
 Givencontraction and cilia sweep
as subcutaneous along
injection to stimulate follicular
 Any tubal damage (as before), endometriosis, cervical problems or sexual growth problems influence this.
 PCOS: low dose step up regimen to increase every 5-7
days until the ovaries respond. Reduce multiple
INVESTIGATIONS: pregnancy by 10%
**COST**  USS follicular development adequate for ovulation at
 Coitus (difficulties with sex) 17mm – artificial stimulation with hCG or LH injection
 Ovulation
 Sperm (functioning poor) Indications for IVF
 Tubal patency o Tubal disease
o Ovulation dysfunction
INDUCTION OF OVULATION: o Endometriosis
o Unexplained infertility
(1) LIFESTYLE MODIFICATION o Male factors
 Folic acid
 Weight loss and stop smoking Complications of IVF
 Correct thyroid abnormality or hyperprolactinaemia o OHSS
o Failed fertilization
(2) CLOMIFENE o Multiple pregnancies or ectopic pregnancy
 Traditional first line limited to 6 months o Fetal abnormality
 Ovulation in 70%, live birth rates 40% o Intra peritoneal haemorrhage and pelvic infection on
 Anti – oestrogen blocking receptors in the hypothalamus and pituitary egg increasing FSH and LH. Only give at the start of cycle on
insertion
day 2 and 6 to initiate follicular maturation
 Monitor clomifene cycles with TVUS in first month to assess ovarian response (increase from 50mg/day to 150mg)
 Also assess endometrial thickness <7mm to indicate success

(3) METFORMIN
 Given if clomifene resistane to increasing effectiveness
 No increasd risk of multiple pregnancyes
 Treats hirsutism in PCOS; prevents development of GDM and early miscarriage

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MENOPAUSE Management of symptoms:

 LMP; retrospective diagnosis after 1 year amenorrhoea
 Average age: 51
 Perimenopause: transition time of fluctuating oestrogen
levels, often starts in early 40s and can last for months
or years. Hormone measurements often normal but
bleeding patterns may change
 Symptoms are due to oestrogen deficiency
 Lifestyle advice – smoking, BMI
 HRT most effective and suitable for majority
 Benefits: symptoms relief, cycle control, bone and cardiac
protection, decreased risk of bowel cancer
OESTROGEN SIDE EFFECTS PROGESTERONE SIDE EFFECTS

Features of menopause:
 CVD increased risk
 Vasomotor: hot flushes & night sweats, palps
 Psychological: mood swings, anxiety
 Joint pains
 Sleep disturbance
 Atrophic vaginitis with itch or burning and urinary
problems; dyspareunia; recurrent infection
 Loss of libido

 Osteopenia (T score -1 and -2.5 SD) and OP (<-2.5 SD)

therefore increasingly prone to wrist; hip; spine #
 Increased risk with early menopause; previous #;
parental # hip; chronic exogenous steroid use; prolonged
immobilization; low BMI; RA; NMD; Hyperthyroidism;
Hypogonadism; Malabsorption syndromes; Liver disease

Premature menopause:
 <40, 1 in 100
 Usually idiopathic; can be autoimmune
 Genetic: Turners syndrome, fragile X
 Iatrogenic: surgery, radiotherapy, chemo
 Long term use of HRT recommended until early 50s.
Women referred to specialist clinic for accurate advice.
 Fertility: IVF with donor eggs, but spontaneous
conception can occur

 Investigations:
o Bimanual & speculum
o Cervical smear
o TVUS for endometrial thickness
o If >4mm hysteroscopy & Bx OP ?cysts/ fibroids/ Ca

o No bloods required >45.

o Younger: 2 occasions with increased FSH 30IU/L
(measure day 2 and 5 of cycle to avoid mid cycle pre-
ovulatory increase and luteal phase suppression of
FSH)
o TFTs (DDx to hot flushes)
o 24 hour levels of catecholamines & 5-
hydroxyindolacetic acid (phaeochromocytoma and
carcinoid syndrome DDx to hot flushes
o DEXA

UTERINE ABNORMALITIES  Management:

o ESMYA or GnRH analogue (PROSTAP/ ZOLADEX) with add
back HRT restrict to 6 months
o Don’t give this if trying to conceive.
36 o Tranexamic acid; COCP for menorrhagia
o Hysteroscopy (Transcervical resection or Intrauterine
morcellator: TRUCLEAR if <3cm)
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 80% anteversion; 20% retroverted.

FIBROIDS
 Benign tumour of myometrium: leiomyomatoma
 25%, common with menopause, FHx, Afro-Caribbean
 Less common in Para1+ and COCP; injectable P
 Oestrogen dependent growth hence regression post menopause

 Intramural, subserosal and submucosal

 Whirled appearance: circumscribed pseudocapsule
 Presentation: 50% asymptomatic. Menorrhagia in 30%. IMB if submucosal/polypoid. Dysmenorrhoea with torsion, red
degeneration or sarcomatous change. Pressure symptoms: urinary urgency, frequency or retention +/- hydronephrosis. Subfertility
or miscarriage

 Complications: slow enlargement.

 Calcifications after menopause if on HRT which may stimulate further growth.
 Hyaline or cystic changes: soft and partially liquified
 Torsion and pain if pedunculated fibroid.
 0.1% leiomyosarcomata potential
 In pregnancy risk of transverse lie, premature and obstructed labour or PPH.
 Post-partum: risk of pedunculated fibroid torsion
 Red degeneration common with severe pain. DON’T REMOVE in caesarean section as can bleed heavily.

 Investigations:
o USS
o Laparoscopy
o Hysteroscopy
o Check Hb if bleed; can be high as fibroids secrete EPO

OVARIAN ABNORMALITIES  Secondary tumour: mets from breast of GI (KRUKENBERG with

 Ovarian masses are commonly silent
 Urgent: Rupture of cyst with intense pain.
Haemmorhage into cyst or peritoneal cavity with pain
orshock. Torsion with infarction of ovary
OVARIAN TUMOUR
 th
1:50 lifetime risk; 4 commonest cancer in women
 Highest rate 80-84
 OCP, pregnancy and lactation protective
 Risk factors:
o Early menarche and late menopause
o Nulliparous.
90% epithelial tumours:
o Serous cyatadenocarcinoma (50%)
o Mucinous cystadenoma (large 10%)
o Endometrioid carcinoma (25%)
o Clear cell carcinoma (<10% and poor Px)
o Brenner tumour (rare, small and benign)
signet ring cells)
 Late presentation: usually with distended abdomen +/- ascites.
Pressure symptoms. Early satiety and change in appetite, weight
loss++
 BRCA 1&2 and HNPCC with 1st degree relative
 Investigations:
o Ca125 screening (>35)
o Ca125 is also raised in fibroids, pregnancy, ectopics, benign cysts,
inflammatory disorders – PID, endometriosis, appendicitis, as well as
heart, kidney and liver failure
o RMI: U x M x Ca125.
o Raised AFP and hCG in germ cell tumours
o MRI for staging.
FIGO STAGING:
o Stage 1 (5 year survival 70%)- confined to ovaries
o Stage 1a: limited to 1 ovary, capsule intact, no tumour on
surface with –ve washings.
o Stage 1b: tumour involves both ovaries, otherwise 1a
o Stage 1c: 1 or 2 ovaries, and on surface & ascites

 Adenocarcinoma spreads directly to pelvis and abdomen with
transcoelomic spread
 Lymphatic spread can also occur
o Stage 2 (5 year survival 40%) – confined to pelvis (2a- locally to
FT or uterus; 2b other tissues; 2c- all & ascites)
o Stage 3 (5 year survival 20%) – confined to abdominal cavity
usually omentum or retro-peritonal nodes
o Stage 4 (5 year survival 5%) – intrahepatic lesions, pleural
37 effusions or mets

 Management
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10% germ cell tumours & sex cord tumours:

 Teratoma or dermoid cyst: younger females <30, small bilateral and asymptomatic until rupture. Fully differentiated tissue of all
cell types

 Dysgerminoma: equivalent to seminoma. Younger and sensitive to radiotherapy

 Granulosa cell tumours: post-menopausal and slow growth. Secrete oestrogen and inhibin causing endometrial hyperplasia –
presenting with PMB. Inhibin is a tumour maker for its recurrence

 Thecomas: Oestrogen and androgen secretion

 Fibroma: benign
 MEIGS SYNDROME – ascites and right pleural effusion with small ovarian mass

Bacterial vaginosis (polymicrobial)

GENITOURINARY MEDICINE
Vaginal discharge
 Physiological with age, hormones (cyclical and
exogenous contraception), pregnancy, personal hygiene,
menstruation and malignancy
 Pathological with infective cause (candida, CT, NG, BV,
TV) or PIC, sepsis, post op infection
 Chemical irritation, allergic response, retained tampon
or condom, IUD, endocervical polyp or ectropion,
atrophic.
 Mixed flora overgrowth of anaerobes including gardnerella
 Presentation: Fishy odour, increasing after unprotected sex
and menstruation
 12% women with multiple partners, IUD or black ethnicity.
 AMSELS Dx CRITERIA:
o Vaginal pH >4.5
o Homogenous grey frothy discharge
o +ve amine or WHIFF test where 10% KOH gives fishy
odour
o CLUE CELLS on wet mount
 Treatment: Metronidazole (oral or cream) OR Clindamycin

General candidiasis (Candida albicans) – THRUSH
 Association with diabetes, antibiotics, pregnancy and
immunosuppression
 DDx to eczema or psoriasis
 Non-sexual transmission
 Presentation: ITCH and COTTAGE CHEESE discharge and
ODOUR; external dysuria and superficial dyspareunia
 Examination: red erythematous, excoriation of vulva,
swelling of labia and lichenification.
 Vulvovaginal candidiasis causes vulvitis
 Diagnosis: Wet mount microscopy (SWAB) and cultures.
Budding hyphae and spores
 Treatment: Butoconzole or Clotrimazole cream or
pessary (CANESTEN) or Nystatin pessary.
Oral fluconazole if recurrent
Trichomoniasis (TV – flagellated protozoa: less common)
 IP of 7 days, sexual transmission
 Presentation: Assymptomatic in 30-50% or profuse, frothy or
watery yellow discharge. Vulvar irritation or oain. External
dysuria and superficial dyspareunia
 Examination: Strawberry Cx
 Diagnosis: Wet mount microscopy and cultures
 Treatment: Oral metronidazole, screen contacts and Rx, test of
cure at 1/52.
Chlaymydia (D to K)
 Presentation: ASSYMPTOMATIC (80%) or urethritis with
dysuria and discharge. Can also get epididymorchtis/ proctitis
 REITERS SYNDROME: urethritis, conjunctivitis and arthritis.
 Diagnosis: PCR urine (nucleic acid amplification test NAAT) –
urine sample clean catch or high vaginal swab

38 Treatment: azithromycin and doxycycline

Gonnorhoea
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 Gram –ve diplococcus
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Syphillis (Troponema pallidum) – developing world

 Primary 2-6wk: Painless vulval ulcer (chancre)
 Untreated secondary: weeks later – rash or flu like and warty genital or perioral growth
 Latent syphilis
 Tertiary: rare – aortic regurgitation, dementia, tabes dorsalis, gumnata on skin
 High risk of congenital infection
 Diagnosis: VDRL test of syphilis EIA

 Treatment: IM penicillin

Genital Herpes (HSV type 2; type 1 cold sores)

 IP of 1-2wk; dormant in dorsal root ganglia where 75% reactivate – localized tingling, less severe recurrence
 Presentation: Local lymphadenopathy and dysuria
 Examination: Multiple small painful vesicles and ulcers
 Uncommon complications: aseptic meningitis, secondary bacterial infection, acute urinary retention
 Treatment: Aciclivor

Non-specific urethritis
 Excess PMNLs in anterior urethra
 Investigate for CT and NG. Presume STI

Salpingitis (Acute PID) +/- endometritis

 Risk factors:
o Young
o Low SE
o Sexually active
o Primigravida
o No barrier contraception
o Multiple partners
 90% ascending infection: chlamydia mostly, gonorrhea, anaerobes, mycoplasma, descending infection, complication of child birth
or miscarriage
 Presentation: Assymptomatic and subfertility or menstrual problems. Commonly BILATERAL LOWER abdominal pain with deep
dyspareunia. PCB, IMB and discharge, backache

 Investigations: Pregnancy test. Endo-Cx swabs for CT and NG; cultures if pyrexic, WBC and CRP increased, pelvic USS excludes
abscess or cyst.
 Management: Analgesia. IM Ceftriazone then doxycycline & metronidazole. ASSESS PARTNER

 Rare complication: Fitz Hugh Curtis syndrome – perihepatic abscess – violin string adhesions. Presents with severe RUQ pain worse
on inspiration and coughing, radiating to the right shoulder
 Increased risk of ectopic pregnancy

Genital warts
 HPV 6 + 11
 Not protected by the vaccine
 Vulval warts

 Treatment: podophyllin, imiquimod cream, cryotherapy if resistant

CONTRACEPTION (2) Mini/ progesterone only pill

 1.2
 5% 16-50
 380mg norethisterone (Micronor): every day without a break
and at same time +/- 3hrs.
 Cerazette: higher dose desogestrol – 95% inhibits ovulation,
39
+/- 12hr with lower ectopic risk.
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 Mode of action: alters cervical mucous and endometrium,
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(1) Combined OCP

 0.16
 Indications:
o Menarche to 50 with no CVS risk
o Menstrual cycle control and dysmennorhoea
o PMS
o Acne

 Mode of action: Inhibition of ovulation by negative feedback on gonadotrophin release

 3wk:1wk for small bleed
 Monophasic pill (Microgynon 30, Yasmin, Dianette – PCOS, hirsuitism however higher thromboembolic risk) with same dose daily.
 Synthetic, ethinyloestradiol and levonorgestrel. Zoely (lower oestrogen content)
 Diphasic/triphasic pill with altering doses

 Investigations prior to starting:

o BP
o BMI
o Pregnancy test
o Chlamydia

 Decreased absorption with V&D and some antibiotics (cephalosporin, pen, tetracycline) – missed pill instructions.
 May need increased dose oestrogen with anti-convulsants or St Johns Wort

 Indications: Start day 1 of each cycle (1st day period)

 Missed pill:
o Can miss 1-2 standard, 1 low dose
o Take as soon as possible and continue as normal.
o 2+ missed, continue and use condoms 7 days
o 7+ missed, avoid break and continue to next packet

 Stop 4 weeks prior to surgery.

 Absolute countraindications:
o Smoker
o BMI >35
o Systolic BP >95
o Hx CVD
o Hx migraine with aura (vasospasm theory)

 Minor SE: nausea, mood, headache, breast tenderness and breakthrough bleeding
 Major SE: VTE and MI, focal migraine, HT, jaundice, liver, cervical and breast cancer
 Protective to endometrial and ovarian cancer

EMERGENCY CONTRACEPTION LARC (Long acting reversible contraception)

(1) Morning after pill (1) Mirena coil

 Levonelle 1500: 3 days with <1% failure  0.1
 EllaOne: 5 days  Progestogen only
 Levonorgestrol 1.5mg  Change mucous and utero-tubal fluid to impair sperm
migration and endometrial changes No implantation
 Progesterone receptor blockers delaying LH surge; best
at ovulation
 Affects sperm function and endometrial receptivity
 Side effects: vomiting, headache and menstrual upset
next cycle
 May interact with some drugs (need to increase dose)

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and can’t use EllaOne more than once in cycle.

(2) Copper IUD

 0.8
 MOST EFFECTIVE with 2 per 1500 failure
 If >72hr since unprotected, prevents implantation as copper is toxic to sperm and blastocyst
 Up to 5 days after expected day of ovulation

STERILIZATION

(1) Filshie clip – laparoscopically under GA

(2) Trans-cervical sterilization – microinserts placed hysteroscopically into fallopian tube(Essure)

0.5% failure rate, must be certain of no further pregnancies. 1 in 200 risk.
Increased risk of ectopic pregnancy.

(3) Vasectomy – more effective (1 in 2000 lifetime)

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