O&G Flashcards
What does a CTG measure and how?
- Foetal HR using ultrasound
- Uterine contractions by measuring the tension of the maternal abdominal wall
CTG mnemonic - DR C BRAVADO
DR – Determine Risk C – Contractions BR – Baseline rate A – Accelerations V – Variability D – Decelerations O – Overall assessment
Why is an abnormal antenatal CTG more worrying than an abnormal labour CTG?
In the antenatal period, the baby is not in a stressful situation, so abnormality will indicate that it is compromised for other reasons
(however, abnormal labouring CTG also needs action)
Why is interpretation of CTG important?
Misinterpretation of the CTG can lead to hypoxia and irreversible brain damage
CTG - Define Risk
Pregnancies can be considered high risk due to:
- Maternal illness – gestational diabetes, hypertension, asthma
- Obstetric Complications – multiple gestation, post-date gestation, Previous CS, IUGR, PROM, congenital malformations, oxytocin induction/augmentation of labour, pre-eclampsia.
- Other risk factors – absence of prenatal care, smoking, drug abuse.
CTG - Contractions
Record the number of contractions present in a 10-minute period
Assess contractions for the following:
- Duration: How long do the contractions last?
- Intensity: How strong are the contractions (assessed using palpation)?
CTG - Baseline Rate
= the mean level of the FHR when this is stable
Normal range = 110 – 160 bpm
Gestational appropriateness – the baseline rate lowers as foetal age advances and the nervous system matures.
Identify foetal tachycardia or bradycardia
What is considered foetal tachycardia?
What are the causes?
= a baseline heart rate greater than 160 bpm
Causes of foetal tachycardia include: • Maternal tachycardia, dehydration and pyrexia – always suspect intrauterine infection. • Foetal hypoxia • Chorioamnionitis • Hyperthyroidism • Foetal or maternal anaemia • Foetal tachyarrhythmia
What is considered foetal bradycardia?
When is this normal?
What are more worrying causes?
= a baseline heart rate of less than 110 bpm
It is common to have a baseline heart rate of between 100-120 bpm in the following situations:
- Postdate gestation
- Occiput posterior or transverse presentations
Severe prolonged bradycardia (more than 3 minutes) indicates severe hypoxia.
Causes of prolonged severe bradycardia include:
- Prolonged cord compression
- Cord prolapse
- Epidural and spinal anaesthesia
- Maternal seizures
- Rapid foetal descent
What should be done if severe foetal bradycardia >3 mins?
emergency buzzer, requires immediate actions and preparation for delivery to prevent irreversible damage from hypoxia.
CTG - accelerations
An abrupt baseline rate increase of 15 beats or more, for 15 secs or more
The presence of 2 or more in a 20-minute period is reassuring
Accelerations occurring alongside uterine contractions is a sign of a healthy foetus.
Accelerations are absent when foetus is sleeping, in chronic hypoxia, drugs and infection
CTG - variations
Bandwidth variation of the baselines – excluding accelerations and decelerations
- Normal – 5-25 bpm (reassuring)
- Reduced – <5 bpm (non-reassuring)
- Saltatory (Increased) – >25 bpm – (non-reassuring)
Causes of reduced variability on CTG
- Foetal sleeping (most common cause) – this should last no longer than 40 minutes
- Foetal acidosis (due to hypoxia) – more likely if late decelerations are also present
- Foetal tachycardia
- Drugs – opiates, benzodiazepines, methyldopa and magnesium sulphate
- Prematurity – variability is reduced at earlier gestation (<28 weeks)
- Congenital heart abnormalities
CTG - decelerations
= an abrupt decrease in the baseline foetal heart rate of greater than 15 bpm for greater than 15 seconds
Can be classified as early, variable or late
Early decelerations on CTG
“Baroreceptor Decelerations”
Start when the uterine contraction begins and recover when uterine contraction stops.
Due to increased foetal intracranial pressure causing increased vagal tone.
These are PHYSIOLOGICAL, not pathological.
Variable decelerations on CTG
= fall in baseline FHR with a variable recovery phase
Variable in their duration and may not have any relationship to uterine contractions
Most often seen during labour and in patients with reduced amniotic fluid volume
Usually caused by umbilical cord compression
Any accelerations before and after a variable deceleration are known as the SHOULDERS of deceleration.
=> Their presence indicates the foetus is not yet hypoxic and is adapting to the reduced blood flow
Late decelerations on CTG
“Chemoreceptor Decelerations”
Begin at the peak of the uterine contraction and recover after the contraction ends.
Indicates there is insufficient blood flow to the uterus and placenta – causing foetal hypoxia and acidosis.
When is a deceleration of FHR considered prolonged?
= a deceleration that lasts more than 2 minutes.
If it lasts between 2-3 minutes, it is classed as non-reassuring.
If it lasts longer than 3 minutes, it is immediately classed as abnormal
Sinusoidal CTG pattern
smooth, regular, wave-like pattern
rare, but very concerning
associated with high rates of foetal morbidity and mortality
usually indicates one or more of the following:
- Severe foetal hypoxia
- Severe foetal anaemia
- Foetal/maternal haemorrhage
CTG - Overall impression
is the overall impression either reassuring, suspicious or abnormal?
What generates the CTG FHR features
- Autonomic Nervous System – involuntary
- Generates a baseline
- Interplay between sympathetic and parasympathetic nervous systems generates variability. - Somatic Nervous System – voluntary
- Transient activity causes changes to HR
- Generates accelerations.
Decelerations in antenatal CTG
reflect hypoxic insult – always abnormal in antenatal CTG
- Poor placental perfusion
- Maternal complications
- Acute events – abruption/cord prolapse
What is the rough total weight gained in pregnancy?
= ~12 kg.
Most of this in the last 20 weeks
What contributes to weight gain in pregnancy?
- Foetus ~3.5kg,
- Placenta ~600g,
- Uterus ~900g,
- Breasts ~400g,
- Blood ~1.2kg,
- Fat ~2.5kg,
- Extracellular fluid ~2.6kg
Physiological changes in pregnancy - the uterus
Undergoes Hypertrophy and Hyperplasia
=> 50 Grams to 950 Grams
Distension after 20th week
=> Leaves pelvis and enters abdominal cavity.
=> Abdominal content is displaced
=> After 38th week fundus descends to prepare for delivery.
Vessels undergo Hypertrophy and coiling
Physiological changes in pregnancy - cervix and vagina
Softening of cervix
Cervical mucous plug
=> Acts as a “seal” for the uterus – protect from ascending infection
Vagina:
- Mucosa thickens
- Increased vaginal discharge
- Increased blood supply
- Becomes more elastic in 2nd trimester
Increased infections – e.g. Candidiasis
Physiological changes in pregnancy - CV changes
Increased blood volume
Physiological anaemia – RBCs diluted due to the increase in plasma volume (no change in MCV)
Heart rate increases (normally not beyond 100bpm)
Increased cardiac output = increased HR x increased SV
Decrease in Systemic Vascular Resistance
- Vasodilatory effect of progesterone
- 10-15mmHg decrease in both SBP and DBP initially
- Tends to return to baseline in the 2nd half of pregnancy
What % increase in maternal blood volume is there when pregnancy reaches term?
~45-50% increase at term
Plasma increase of 50% and RBC 30%
How much as cardiac output increased by the time a pregnancy reaches term?
CO = 30-50% above baseline by term
Normal CVS Signs in Pregnancy
Tachycardia, collapsing pulse Distended neck veins, JVP is normal Oedema Displaced, diffuse apex beat Loud S1 and S3 Systolic ejection murmurs Ectopics (Atrial and Ventricular)
Abnormal CVS Signs in Pregnancy
Apex displaced by 2 cm Diastolic murmurs Pan-systolic murmurs Ejection systolic murmurs that are grade 2/6 or greater Raised JVP
Physiological changes in pregnancy - haematological changes
Mild pro-thrombotic state created – less chance of bleeding during birth, but increased chance of VTE
Physiological changes in pregnancy - respiratory changes
Increased AP and transverse diameters of thoracic cage
Upward displaced diaphragm (due to enlarging uterus)
Progesterone causes bronchodilation
Increased oxygen demand (due to increased maternal metabolism and foetal demands)
Decrease in:
- Residual Volume
- Total lung capacity
Increase in:
- RR (by 1-2 breaths, tachypnoea is a red flag in pregnancy)
- Tidal Volume
Slight decrease in PaCO2, increase in PaO2, slight change in pH (respiratory alkalosis)
Why is there a change in PaCO2/PaO2 in pregnancy?
This facilitates the transfer of oxygen from mother to foetus and the transfers of carbon dioxide from foetus to mother.
Physiological changes in pregnancy - renal changes
Increased renal blood flow by 75%
Increased GFR
Physiological hydronephrosis and hydroureteronephrosis
=> Predisposes to infection
Physiological proteinuria and oedema
Renin, EP and 1,25 DHCC increase
In the third trimester when the foetus starts to engage in the pelvis, there is an increased frequency of urination and there can be incontinence.
What happens as a result of increased glomerular filtration which occurs in pregnancy?
=> Increased creatinine clearance, protein/albumin excretion, and urinary glucose excretion
=> Serum creatinine and albumin levels fall
=> Proteinuria
Physiological changes in pregnancy - GI changes
Progesterone causes smooth muscle relaxation which slows down GI motility and decreases lower oesophageal sphincter (LES) tone.
=> Constipation and Reflux.
Nausea and vomiting (“morning sickness”)
Haemorrhoids
Physiological changes in pregnancy - Thyroid changes
Beta-HCG causes thyroid stimulation, due to its structural similarity with TSH.
=> Causes a decrease in serum TSH in 1st trimester.
Increased renal clearance and foetal uptake induce a relative deficiency in circulating iodide.
Increased thyroid-binding globulin (TBG)
Increased total T4 and T3 (but normal Free T4 & Free T3)
Importance of maternal thyroid function in pregnancy
The foetal thyroid begins concentrating iodine and synthesizing thyroid hormones after 12 weeks of gestation
=> Before this time any thyroid hormones are supplied by maternal reserves, in order to promote the physiological foetal brain development.
Physiological changes in pregnancy - Adrenal changes
Increase in:
- Corticosteroid-binding globulin, Total and Free cortisol
- Renin, Angiotensin II, and Aldosterone
No change in:
- Catecholamine levels
- Normal diurnal variation of ACTH
Physiological changes in pregnancy - Pituitary changes
Increase in:
- Gland volume
- Prolactin Levels
- Placental GH and Human placental lactogen (hPL)
Undetectable LH and FSH
Physiological changes in pregnancy - changes in calcium metabolism
Increased placental flux of Ca2+ to meet foetal requirements
Increased Ca2+ absorption from gut
Increased DHCC and PTH
Physiological changes in pregnancy - skin changes
General darkening and glowing
Breast enlargement and preparation for lactation
Montgomery tubercles
=> Sebaceous (oil) glands that appear as small bumps around the dark area of the nipple.
Increased areola pigmentation
Spider naevi
Chloasma of pregnancy
Linea Nigra
Striae Gravidarum
what is Chloasma of pregnancy ?
= Hypermelanosis of sun-exposed areas
What is linea nigra?
Linear hyperpigmentation that commonly appears on the abdomen
Attributed to increased melanocyte-stimulating hormone made by the placenta
What are the “3 P’s” of normal delivery?
- Passage (pelvis of the mother) must be adequate in terms of size and shape
- Powers (contractions) should be regular and strong
- Passenger (foetus) should be in the correct position, well flexed and not too large in relation to the maternal pelvis.
How does the pelvic width vary?
Pelvic inlet = widest in its transverse direction.
Mid-cavity = circular
Pelvic outlet = widest in the antero-posterior direction
Importance of the pubic arch in obstetrics
important to measure as if it is too narrow then vaginal delivery will be difficult/impossible.
Importance of the sacral promontory in obstetrics
Measuring the distance between this and the pubic symphysis is known as the obstetric conjugate and should be ~10cm
Importance of the ischial spine in obstetrics
used as a reference point to determine the station of the foetal head (or presenting part)
Foetal skull - anterior fontanelle
- Diamond shaped.
- Bound by the frontal and parietal bones.
- The frontal, coronal and sagittal sutures come together at this fontanelle.
- The anterior fontanelle is the anterior boundary of the vertex of the foetal skull.
Foetal skull - posterior fontanelle
- Triangular in shape.
- Bound by the occipital and parietal bones.
- The sagittal and lambdoidal sutures come together at this fontanelle.
- It is the posterior landmark for the vertex of the foetal skull
What is caput?
What might this indicate?
swelling on the scalp of foetus
may suggest labour is obstructed
What is moulding?
What might this indicate?
crossing of the foetal parietal bones
may suggest labour is obstructed
Occiput presentation of foetal head
classified according to the position of the occitput in relation to the maternal pelvis – e.g. occipto-anterior, occipito-transverse
What part of the foetal skull most commonly presents?
the vertex
Brow presentation of foetal head
on VE - can very easily feel the orbital ridges above the foetal eyes.
This presentation cannot deliver vaginally unless the foetus extends its head to become a face presentation or flexes to become a vertex presentation
Face presentation of foetal head
the position is classified according to the position of the chin (mentum) in relation to the maternal pelvis e.g. mento-anterior, mento-posterior
What is the most favourable position of the foetal head for delivery?
Occipitoanterior = most favourable
You can deliver in the occipitoposterior position, but this is more difficult as the diameter of the head in this position is larger.
What are the signs of labour?
CONTRACTIONS
Regular, painful uterine contractions – every 2-3 mins, lasting 45-60 seconds.
RUPTURED MEMBRANES
SROM = spontaneous rupture of membranes
DILATED CERVIX
identified on vaginal examination
Reasons for admission when labour is starting
- Established labour (regular contractions)
- ROM
- Bleeding
- Green discharge
- Mother feels unwell
- Foetal movements stop
- Strong urge to push
Reasons for staying at home until labour is fully established
to reduce iatrogenic risk/unnecessary interventions
What are the stages of labour
Latent phase - dilatation <4cm
1st stage - from established labour to full dilatation
2nd stage - from full dilatation to delivery of the baby
3rd stage - from delivery of baby to separation and delivery of placenta and membranes
What happens in the latent phase of labour?
Irregular contractions
Can be short lasting and not as painful
Cervical change, with dilatation <4cm
May stop and start, can last for a number of days
What happens in the 1st stage of labour?
What is the expected progress?
Regular, painful contractions (3-4 every 10 mins)
Cervical dilatation 4cm => 10cm
Expected progress – 0.5cm (Primips) or 1cm (Multips) cervical dilatation per hour.
What happens in the 2nd stage of labour?
How long does it last?
Passive = no pushing, to allow further descent of the head.
Active = pushing
No longer than 2 hours (primips) or 1 hour (multips) active second stage.
What happens in the 3rd stage of labour?
How long does it last?
Delivery of placenta
(meanwhile: cord clamping, skin to skin, neonatal vitamin K, early feeding).
- Physiological = no drugs
- Active = IM syntometrine (oxytocin analogue) to induce placental separation.
Normally ~15 mins (no longer than 60 mins if physiological, or 30 minutes if active = retained placenta).
How is cervical dilatation monitored in labour?
What is the expected progression of dilatation?
regular vaginal examination every 4 hours (up to 7cm, more frequently after 7cm) to ensure adequate progress.
Progress should be at least:
- 0.5cm per hour for primps
- 1cm per hour for multips
Maternal monitoring in labour
Low-risk pregnancy – suitable for midwifery-led care.
High-risk pregnancy – requires consultant-led care
All women will have regular observations in labour (every 4 hours) – BP, RR, temperature, urine output
Foetal monitoring in labour
FHR is recorded every 15 minutes as part of the basic observations, and also monitored after contractions
=> If low-risk, offer intermittent auscultation of the foetal heart
=> If high-risk, offer continuous cardiotocograph (CTG).
=> Foetal scalp electrode if needed
Liquor colour – check for meconium
What factors put the foetus at high risk and CTG should be offered?
Foetal growth restriction, Reduced movements, Maternal medical conditions, Smoking, etc.
What factors might lead to a CTG being started later in labour?
abnormal FHR,
labour >5 hours,
high risk labour,
meconium
What factors when monitoring the foetus in labour might indicate the need for emergency C-section?
Bradycardia >3mins = C-section
pH <7.20 or BE
Process of normal birth
Head free in maternal abdomen before engagement.
Foetal head flexes and contractions allow descent of foetus.
As the head descends it will undergo INTERNAL ROTATION to occipitoanterior (OA).
As the foetal head is delivered though the pelvic outlet, it will undergo extension.
Once the head has delivered, the foetus undergoes restitution (EXTERNAL ROTATION) where the head realigns with the body.
Delivery of anterior shoulder, followed by posterior shoulder and the rest of the baby with the next contraction.
What pain relief options are there in labour?
Entonox (gas and air)
TENS
Systemic opioids (Morphine/pethidine)
- Given IM by midwife/doctor
- Mild analgesia, fairly rapid onset
Epidural (fentanyl and bupivacaine)
What are the side effects of systemic opioids in labour?
N&V, sedation, crosses placenta (respiratory depression in baby)
Where is an epidural injected?
What does this achieve?
Injected by anaesthetist into epidural space between L3 and L4.
Achieves complete sensory (except pressure) & partial motor blockade from injection site downwards
What problems are associated with an epidural?
- Hypotension
- Itching/toxicity
- Urinary retention (due to reduced sensation)
- Poor mobility
- CSF tap (if inserted too far), causes headache
- Complete spinal analgesia
- Reduced ability to push.
What are indications for an epidural?
- Long labour
- Twins
- Pre-eclampsia (reduces BP)
- For instrumental delivery/C-section
What are contraindications for an epidural?
- Sepsis
- Coagulopathy
- Spinal abnormalities/neurological disease
Bishop’s score
indicates likelihood of IOL success
- High score – cervix favourable, associated with an easier/shorter induction
- Low score – cervix unfavourable, takes longer and more likely to fail. May end in LSCS
Indications for induction of labour
Term +10 Multiples Pre-eclampsia Diabetes/GDM IUGR PROM = prelabour term ROM
Methods of induction of labour
Membrane Sweep – use fingers to separate membranes from cervix/uteris
Prostaglandin E2 gel (Propess) – into posterior vaginal fornix.
Amniotomy (+ oxytocin if no induction after 2 hours)
Oxytocin (following amniotomy OR if membranes are already ruptured)
Complications of IOL
- Slow labour (insufficient uterine activity)
- Cord prolapse
- Infection
- Postpartum haemorrhage
Contraindications to IOL
- Abnormal lie
- Placenta Praevia
- Pelvic obstruction
- Previous C-section(s)
What can cause poor progress in labour?
POWER Dehydration/ketosis Maternal exhaustion Epidural/other medication Overactive uterus
PASSENGER Twins (or more) Abnormal presentation (breech/brow) Abnormal position (OP/OT) Macrosomia
PASSAGE
Size & shape of pelvis
Pelvis deformities
Cervical abnormalities
What is the most common cause of slow progress in labour?
Insufficient uterine activity
Augmentation in Labour
If dilation <1cm/hour in active phase:
- Amniotomy (AROM) using amniohook.
- Oxytocin Drip
- C-section – if failed to reach 10cm after 12 hours.
If pushing for >1 hour (multips) or >2 hours (primips) and delivery not imminent:
- Assisted Vaginal Delivery
- C-section – after 2 failed attempts of assisted delivery.
Indications for assisted vaginal delivery
- Prolonged second stage
- Acute bradycardia at full dilatation
- Pathological CTG at full dilatation
What are the pre-requisites for an assisted vaginal delivery?
- Fully dilated
- > 34 weeks
- Cephalic presentation
- Head below the ischial spines
- Maternal consent gained
- Adequate analgesia (epidural, spinal or pudendal nerve block)
- Usually requires episiotomy
Types of assisted vaginal delivery
NON-ROTATIONAL - if head in OA position
=> Neville barnes forceps
=> Ventouse
ROTATIONAL - not in OA position
=>Ventouse
=> Manual rotation (using the hand of the assistant) followed by forceps
Complications of C-section delivery
how are these managed?
- Haemorrhage – G&S, XM, transfusion ready
- Infection – prophylactic Abx
- VTE – Prophylactic thrombolysis + TED stockings
- Post-op pain and immobility
- Damage to visceral organs/foetus
- Cannot drive for 4-6 weeks
- Future problems due to adhesions and scarring – risk of placenta previa/uterine rupture
Elective C-Section
- when?
- why?
Usually done at ~39 weeks
Indications: breech, placenta previa, severe IUGR, multiples, diabetes, severe pre-eclampsia
Indications for emergency C-section
failure to progress in labour,
foetal distress
Benefits of C-section
Lowers risk of scar rupture if previous C-section
Lowers risk of perineal trauma
Lowers risk of HIE
Can plan delivery date
Disadvantages of C-section
Longer recovery
Increased risk of bleeding and infection
Increased chance will need C-Section in future.
Benefits of VBAC
- Quicker recovery
- No anaesthetic risk
- Reduced risk of bleeding, infection, VTE
- Increased chance of normal vaginal delivery in future pregnancies.
Risks of VBAC
- Rupture of previous uterine scar – needs emergency C-section
- Increased risk of perianal trauma
Problems with repeat C-section
- Increased complications with adhesions
* Increased risk of placenta previa in future pregnancies
Management of VBAC
• Consultant-led care
• Hospital delivery with: Continuous CTG monitoring Maternal Obs IV access & FBC Pool birth not recommended (but can be discussed with consultant)
• Avoid IOL due to increased chance of scar rupture
Presentation of foetus
= part of foetus occupying lower section of uterus.
- Cephalic
- Breech
Lie of foetus
= relationship of foetus to long axis of uterus
- Longitudinal
- Transverse
Unstable lie = continually changing position
Causes of Abnormal Lie
Preterm labour
Increased room to turn
- Polyhydramnios, high parity (stretched uterus)
Decreased room to turn
- Uterine/foetal abnormalities, multiple pregnancy, oligohydramnios
Prevention of engagement
- Placenta praevia, pelvic tumour
Foetal abnormalities
- IUGR/macrosomia, short cord, hydrocephaly
Management of abnormal lie
< 36 weeks - no action needed (may spontaneously turn)
> 37 weeks – admission and USS to exclude polyhydramnios/ placenta praevia
(External Cephalic Version between 36-38 weeks if expert)
Continued abnormal lie to 41 weeks/labour – C-section
Risk factors for breech presentation
- Previous breech presentation
- Pre-term labour/prematurity
- RFs for abnormal lie
Complications of breech presentation
- Foetal structural/neurological abnormalities
- Cord prolapse
- Late detection of trapped head => foetal hypoxia and death
Management of breech presentation
- External Cephalic Version (ECV): attempt after 37 weeks, 50% successful
- Elective C-Section: advised if ECV failed or contra-indicated.
- Vaginal Breech Birth: if patient chooses over C-section
=> Increased risk of foetal compromise and cord prolapse
External Cephalic Version
No analgesia, but uterine relaxant (tocolytic)
USS-guided manipulation of foetus with hands on abdomen
CTG-monitoring and Anti-D given immediately after
Contraindications to external cephalic version
multiple pregnancy, foetal distress, recent APH/active PV bleed, ruptured membranes, uterine abnormality
Risks of external cephalic version
bleed, foetal distress, uterine rupture, placental abruption
What is Shoulder Dystocia?
When normal downwards traction fails to deliver the shoulders after the head
=> anterior shoulder caught on pubic symphysis
Risk factors for shoulder dystocia
LARGE baby (>4kg) Previous shoulder dystocia High maternal BMI Maternal diabetes IOL/instrumental delivery
Complications of shoulder dystocia
Baby – brain damage, damaged brachial plexus (Erb’s Palsy)
Mum – perineal injury, uterine rupture, PPH
Management of shoulder dystocia
= RAPID SKILLED INTERVENTION
- McRobert’s Manoeuvre – hyperextend legs + suprapubic pressure
- Wood’s Screw manoeuvre – manual internal rotation of shoulders (need episiotomy)
- Grasp posterior arm – gently pull down and rotate body as it follows
- Last resorts – symphysiotomy, Zavanelli manoeuvre, C-section (often too late for this)
SOAPS skilled intervention in obstetrics
- Senior Midwife
- Obstetrician
- Anaesthetist
- Paediatrician
- Scribe
Cord prolapse
When the cord descends below the presenting part
Felt on VE/pathological CTG signs
Risk factors for cord prolapse
- Preterm labour/low birth weight
- Breech/OP/abnormal lie
- Multiples (2nd twin)
- Polyhydramnios
- Multiparous
Complications of cord prolapse
cord compression/spasm => foetal hypoxia
Management of cord prolapse
GET HELP (SOAPS) + Prepare for C-section
- Stop cord compression
- If cord is outside, keep warm and moist but do not force back inside
- Delivery – keep patient on all 4s while prepare for safest delivery
=> C-section usually, but sometimes instrumental.
Uterine Rupture
De novo tear OR opening of previous scar
What predisposes to uterine rupture?
- Scarred uterus
- Neglected obstructed labour
- Congenital uterine abnormalities
Management of uterine rupture
- Maternal resuscitation – IV fluids and blood
2. If blood loss too fast – urgent laparotomy to deliver foetus and repair/remove uterus
Amniotic Fluid Embolism
Liqour enters maternal circulation, causing anaphylaxis
Risk factors for amniotic fluid embolism
Polyhydramnios
Very strong contractions
Typically occurs at ROM, C-section or TOP
Complications of amniotic fluid embolism
- Dyspnoea, hypoxia, hypotension
- Seizures, cardiac arrest, acute heart failure
- DIC, pulmonary oedema, respiratory distress
All above can cause death
Management of amniotic fluid embolism
Maternal resuscitation – IV fluids, O2, blood and FFP for transfusion
Incidence of twin/triplet pregnancies
Twins – 1/80 pregnancies
Triplets – 1/1000 pregnancies
Risk factors for multiple pregnancy
Fertility treatments/ovarian hyperstimulation
Increasing maternal age
Higher parity
Genetics
How are Dizygotic Twins formed?
How common is this form?
fertilisation of 2 different oocytes by 2 different sperm
80% of twins
How are monozygotic Twins formed?
How common is this form?
miotic division of a single oocyte (varies depending on when division occurs)
20% of twins
Different types of monozygotic twin
Dichorionic Diamniotic (DC/DA) = 2 placentas, 2 amnions
Monochorionic Diamniotic (MC/DA) = 1 placenta, 2 amnions
Monochorionic Monoamniotic (MC/MA) = 1 placenta, 1 amnion
Incomplete division – conjoined twins
Twin USS - Lambda-sign
= triangular appearance to chorion insinuating between the layers of the inter twin membrane
Strongly suggests a dichorionic twin pregnancy
Twin USS - T-sign
= absence of lambda-sign
suggests monochorionic twin pregnancy
Maternal complications of multiple pregnancy
Gestational diabetes, pre-eclampsia, anaemia = more common
Spontaneous miscarriage
Preterm labour
Malpresentation of a baby at labour
Prolonged labour
APH/PPH
Foetal complications of multiple pregnancy
Increased mortality/stillbirth Increased chance of handicap Congenital abnormalities (more common in MC twins) IUGR (usually one twin is smaller) IUFD of one foetus
What are some specific complications of Monochorionicity?
Twin-twin transfusion syndrome (TTTS) Twin Reversed Arterial Perfusion (TRAP) Selective Foetal Growth Restriction Co-twin Death Monoamniotic Twin entangled cords
What is twin-twin transfusion syndrome (TTTS)?
What are the outcomes?
Occurs in MCDA only.
Unequal blood distribution through anastomoses in placenta
=> Donor twin – volume depletion, anaemia, IUGR, oligohydramnios
=> Recipient twin – volume overload, polycythaemia, cardiac failure, polyhydramnios
Outcomes:
- Severe pre-term delivery
- IUFD
what is Twin Reversed Arterial Perfusion (TRAP) ?
Foetal blood systems connected
One twin (pump) = normal
Other twin (acardiac) = abnormal/missing heart and upper limbs
Selective Foetal Growth Restriction of twins
Due to superficial artery-artery anastomoses
Intermittently absent or reversed blood flow to 1 twin
Can cause sudden IUFD
Co-twin Death
Death of one twin causes acute transfusion of blood
Results in hypovolaemia => death/neurological damage in surviving twin
Antenatal management of multiple pregnancy
= Consultant-led as high-risk.
- Early USS to determine chorionicity
- Regular USS checks for IUGR
- Selective Reduction
- Birth plan/method of delivery discussed
- Education patient on signs of preterm labour and complications
Selective reduction in multiple pregnancy
Discussed at 12 weeks if triplets or more.
Reduces chance of preterm delivery and associated foetal death/handicap
Intra-cardiac injection of potassium chloride to leave behind only 2 foetuses
How often are USS checks for twins to check for IUGR?
DC twins – every 4 weeks from 28/40
MC twins – every 2 weeks from 12/40
Delivery management of multiple pregnancy
Timing:
=> DC twins = 37 weeks
=> MC twins = 36 weeks
Hospital delivery
=> Consultant, 2x midwives (1 senior), paediatrician
Continuous CTG
Epidural recommended
Mode of delivery!
Mode of delivery of twins
C-section commonly used for any multiple pregnancies (vaginal delivery has more risk for 2nd twin).
NVD = only viable if 1st twin is cephalic presentation
Foetal distress – speed delivery with ventouse or breech extraction.
After 1st twin is born, check lie of 2nd twin (2nd baby may need C-section)
Active 3rd Stage due to high risk of PPH
What are absolute indications for C-section in multiple pregnancy?
- Malpresentation of 1st twin
- Hx of antepartum complications
- Triplets or more
When is the antenatal booking visit?
As early as possible in the pregnancy (before 10 weeks)
What happens at the antenatal booking visit?
Risk assessment
Full Hx taken from the patient by the midwife
Relevant examinations
Routine investigations
Discuss screening and give information
Arrange Dating Scan
What points are important in the booking visit history?
Past obstetric Hx/disorders
Gynaecological Hx – e.g. recurrent miscarriage, uterine surgery
Medical conditions increasing the risk of problems (including psychiatric disorders)
DHx – stop if contraindicated in pregnancy, vits/folate
SHx – smoking, alcohol, illicit drugs, housing/support, safe at home?
What examinations are relevant at the booking visit?
BMI (low or high?)
BP
Urine dip (glucose, protein, leucocytes, nitrites)
Dating Scan
Between 11-13 +6weeks
Check gestation, detect multiple pregnancies
Screen for trisomies (13, 18, 21)
What routine investigations are done at the booking visit?
Blood screen – FBC, blood group & Anti-D antibodies, glucose tolerance, syphilis, rubella immunity, HIV & Hep B, Hb electrophoresis.
Other tests – infection screening (e.g. chlamydia), urinalysis, urine MC&S
When do the regular antenatal visits occur?
16-28 weeks – monthly
28-36 weeks – fortnightly
36 weeks onwards – weekly
What occurs at the regular antenatal visits?
History:
- Brief review
- Physical and mental health check up
- Foetal movements
Examination:
- BP & urinalysis
- Pregnant abdo exam – FHR, lie and presentation
- Symphysio-fundal Height
What occurs at the 28-week antenatal visit?
BP + urine dip
SFH measured
FBC & antibodies checked
OGTT if indicated (e.g. raised BMI, glycosuria)
Anti-D given if rhesus negative
What occurs at the 34, 36, 38, 40 Weeks antenatal visits?
BP + urine dip
SFH measured
Foetal lie and presentation checked
Info given on birth plan and labour
Info give on caring for newborn, etc.
USS – Presentation and Placental location
What occurs at the 41-week antenatal visit?
Offer membrane sweep Discuss IOL (offered at 42 weeks)
Antenatal lifestyle advice
Well-balanced diet, approx.. 2500 kcal.
Avoid unpasteurised milk, soft cheese etc. (risk of salmonella, listeria, toxoplasmosis)
Avoid alcohol (especially in first 12 weeks) Avoid smoking
Exercise – avoid contact sports but swimming, etc. is advised.
Antenatal medication advice
Avoid in first trimester if possible
Folic acid supplementation – 400mcg/day until week 12
VitD supplementation – 10mcg/day if BMI >30 / low sun exposure
Iron supplementation – if anaemic
Vaccines – flu and whooping cough
When is 5mg folate indicated in pregnancy?
- Epilepsy
- Diabetes
- BMI >30
- Hx of baby with spina bifida
When do the routine antenatal USS scans occur?
12 weeks – dating (gestation and nuchal translucency)
20 weeks – foetal anomaly scan
(+36/38 weeks if low lying placenta at 20 week scan)
Why and when do the antenatal serial growth scans occur?
Take place if high risk
4 weekly from 28 weeks – (28, 32, 36 weeks)
2 weekly if monochorionic twins
When can Rhesus sensitisation of Rh -ve mother occur ?
Rh -ve mother and Rh +ve foetus can cause the mother to develop IgG antibodies against foetal RBCs
Can occur after previous birth, amniocentesis, APH/vaginal bleeds, miscarriage, TOP, ectopic, trauma (e.g. fall)
How can Rhesus sensitisation be prevented?
Give Anti-D at 28-weeks +/- within 72 hours of sensitisation event
Risks of alcohol in pregnancy
- Miscarriage
- Reduced birth weight/IUGR
- Intellectual impairment
- Foetal alcohol syndrome
Foetal alcohol syndrome
Small head/eyes, saddle nose, thin lips,
Cerebral palsy, Learning difficulties,
Behaviour/attention problems,
Hearing/vision problems,
Cardiac defects
Risks of Smoking in pregnancy
- Low birth weight/foetal growth restriction
- Preterm delivery
- Miscarriage/stillbirth
Risks of illicit drugs in pregnancy
- Low birth weight/foetal growth restriction
- Preterm delivery
- Cardiac defects (ecstasy)
- Sudden infant death syndrome
- Neonatal withdrawal syndrome (especially opiates and BZDs)
Antenatal blood screening
Blood group and Rhesus Status
Antibodies
Haemoglobinopathies
=> Thalassaemia
=> Sickle cell (depending on ethnic background)
Anaemia
Antenatal infection screening
Rubella immunity
Syphilis
HIV
Hepatitis B
Foetal congenital abnormalities - screening tests
Blood tests
- AFP, b-hCG, PAPP-A, oestriol.
USS:
- Combined test – nuchal translucency, blood hCG and PAPP-A
- Triple test (>14 weeks) – AFP, b-hCG, oestriol
- Foetal anomaly scan at 20 weeks
Foetal congenital abnormalities - what might raised AFP indicate?
NTDs
Abdominal Wall defects
Multiple pregancy
Foetal congenital abnormalities - what might low AFP indicate?
Down’s (trisomy 21)
Edward’s (trisomy 18)
Maternal DM
What might a large nuchal translucency indicate?
= larger risk of structural abnormalities
Foetal congenital abnormalities - non-invasive diagnostic tests
Foetal MRI – diagnose intracranial lesions
3D/4D USS – better visualisation of abnormality
Pre-implantation genetic diagnosis (if IVF)
Foetal congenital abnormalities - invasive diagnostic tests
Amniocentesis
Chorionic Villus Sampling
Amniocentesis - process and risks
- 1% risk of miscarriage
- Removal of amniotic fluid via fine-gauge needle and USS
- Safest after 15 weeks’ gestation
- Diagnosis of chromosomal abnormalities, infection, inherited disease
Chorionic Villus Sampling
- 1-2% risk of miscarriage
- Take sample of placental cells via fine gauge needle.
- Done between 11-13 weeks’ gestation (early enough for TOP)
- Diagnosis of chromosomal abnormalities, inherited disease.
What is the risk of invasive tests for congenital abnormalities?
miscarriage, rhesus sensitisation, infection, foetal trauma
What are some chromosomal abnormalities which can be detected ?
Down's syndrome (Trisomy 21) Edward's Syndrome (Trisomy 18) Patau Syndrome (Trisomy 13) Klinefelter's Syndrome Turner's Syndrome
Foetal Hydrops
excess fluid in 2 or more areas;
(including ascites, pleural effusion, pericardial effusion, and skin oedema)
can result from rhesus antibodies, chromosomal/structural abnormalities, anaemia
Obstetric Haemorrhage - minor blood loss
500 - 1000 mL
Obstetric Haemorrhage - major blood loss
> 1000 mL
What is antepartum haemorrhage?
= bleeding from the genital tract after 24 weeks gestation until labour.
Causes of APH
COMMON
Undetermined
Placental abruption
Placenta praevia
RARER
Genital tract pathology
Uterine rupture
Vasa praevia
What is placenta praevia?
When the placenta is totally or partially inserted in the lower uterine segment (<2cm from internal cervical os):
=> Minor – placenta not covering os
=> Major – placenta partially/fully covering os
Risk factors for placenta praevia
Twins High parity Increased maternal age (>40) Scarred uterus – previous C-section/surgery, previous placenta praevia Smoking
Placenta accreta
= when the placenta attaches itself too deeply and too firmly into the uterus
Placenta increta
placenta accreta, where the placenta attaches itself even more deeply into the muscle wall of uterus
Placenta percreta
= when the placenta attaches itself and grows through the uterus, sometimes extending to nearby organs, such as the bladder
Stage I placenta praevia
Placenta reaches lower segment but not the internal Os
Stage II placenta praevia
Placenta reaches internal os, but does not cover it
Stage III placenta praevia
Placenta covers the os before dilatation, but not when dilated
Stage IV placenta praevia
Placenta completely covers the os, even when dilated
Symptoms of placenta praevia
Intermittent, PAINLESS bleeds (increasing in frequency and intensity)
Abnormal foetal presentation – e.g. breech, transverse lie, foetal head not engaged
What is a cause of PAINLESS bleeding during pregnancy?
placenta praevia
What should you not do to examine suspected placenta praevia?
AVOID VAGINAL EXAMINATION – can provoke massive bleed
Placenta praevia - investigations
TV USS to diagnose
Management of placenta praevia
Presentation without bleeding (asymptomatic) – delivery between 36-37 weeks.
Presentation with bleeding – ADMIT and consider late preterm delivery
Delivery:
=> Elective CS (earlier if severe bleeding)
=> If placenta accreta/percreta – Rusch balloon compression/total hysterectomy after C-section to decrease bleeding.
Placental Abruption
= part or all of the placenta separates from the uterine wall before delivery of the foetus.
~1% of pregnancies
Risk factors for placental abruption
Hx of placental abruption Pre-eclampsia/pre-existing HTN IUGR Multiple pregnancy High parity Autoimmune Smoking/cocaine use
Symptoms of placental abruption
PAINFUL, dark bleeds (amount does not equal severity)
Tender, contracting uterus
If severe – “woody-hard” uterus, hypotension, tachycardia
Decreased foetal movements
Signs of hypovolaemic shock
Concealed placental abruption
Pain without any bleeding
What is a cause of PAINFUL bleeding during pregnancy?
Placental abruption
Management of APH
ADMIT
- FBC, clotting screen, XM (4-6 units), U&Es, Kleihauer test (if mum Rh -ve)
- Hx, including SHx to rule out domestic abuse.
- A-E Assessment (including urine dipstick)
- Abdominal examination
- Speculum/vaginal examination – assess amount of bleeding, cervical appearance
Stabilise the mum before assessing the foetus.
=> CTG for foetal wellbeing
Anticipate PPH
=> Prepare for active 3rd stage to reduce risk
Management of Placental Abruption
No foetal distress, >36 weeks – IOL with amniotomy
No foetal distress, <36 weeks – monitor on antenatal ward, steroids if <34 weeks.
Foetal distress = urgent C-section
=> Intra-operative/PP haemorrhage common
Vasa Praevia
When foetal blood vessels run in the membranes in front of the presenting part, near the cervix.
When the membranes rupture, the foetal vessels do too, leading to a massive foetal bleed.
Symptoms of vasa praevia
Moderate, PAINLESS vaginal bleed when/after membranes rupture (amniotomy or spontaneous)
Severe foetal distress
Management of vasa praevia
Urgent C-section (usually too slow to save foetus)
Uterine Rupture as a cause of APH
Occasionally rupture occurs before labour in women with scarred/congenitally abnormal uterus.
=> Signs of hypovolaemia => Sudden onset abdo pain => High foetal presenting part => Uterine contractions may cease => Bleeding (can be concealed) => Haematuria (scar can involve the bladder) => Pathological CTG
= obstetric emergency
APH - Bleeding of Gynaecological Origin
- Cervical carcinoma – suspect if small recurrent/post-coital bleeding
- Cervical polyps
- Ectropions
- Vaginal lacerations
Primary PPH
= Loss of >500mL blood within 24 hours of delivery
or >1000mL after C-section
What are the 4T’s as causes of PPH?
TONE – uterine atony (90% of PPH)
TRAUMA – vaginal/cervical tears, episiotomy
TISSUE – retained placenta, retained blood clots, placenta accreta
THROMBIN (coagulopathies) – congenital disorders, anticoagulation, DIC, pre-eclampsia
What are the risk factors for uterine atony?
prolonged labour, grand multiparity, fibroids, overdistension (multiples, polyhydramnios), muscle relaxants
Prevention of PPH
Identify high-risk women in antenatal visits
Active management of 3rd stage of labour – Syntometrine for placental delivery
Management of primary PPH
- GET SENIOR HELP (obstetric emergency)
- Resuscitation – O2, XM and FBC
=> Transfuse blood as soon as possible (activate obstetric major haemorrhage call)
=> Catheter to monitor input and output - Identify cause – abdo palpation, VE, examine placenta, USS
- Treat cause:
- Retained placenta – remove manually if bleeding/not delivered in 60 minutes
- Uterine atony – IV oxytocin/ergometrine to contract uterus; PGF2A if persists
- Persistent haemorrhage – surgery
Secondary PPH
= Excessive blood loss between 24 hours and 12 weeks after delivery.
Caused by endometritis +/- retained placental fragments.
Sometimes can be due to poor healing of a perineal tear
What is the agent of choice in managing PPH?
Syntometrine/Syntocinon
=> 5 unit slow IV bolus
=> Sustained effect use with 40u infusion (in 500ml saline)
Side effects of syntometrine
Vasodilation (hypotension) and reflex tachycardia
Use of Ergometrine in PPH
125mcg-500mcg IV or IM
SEs – Nausea and vomiting, HTN, coronary spasm, ischaemic pain
Contraindicated in hypertensive patients
Surgical management of PPH
Treat cause and early transfer to theatre if needed.
No statistical difference among the outcomes of the various available surgical methods
- Uterine balloon tamponade
- Compression sutures
- Arterial ligation
- Aortic clamping
- Hysterectomy/Subtotal hysterectomy
Transexamic acid in PPH
Effective anti-fibrinolytic;
Consider in cases where blood loss is major and ongoing
The HPG-axis
Hypothalamus secretes GnRH
GnRH promotes the release of LH and FSH from the anterior pituitary.
LH and FSH travel in the bloodstream to the ovaries. When LH and FSH bind to the ovaries they stimulate the production of oestrogen and inhibin
Increasing levels of oestrogen, progesterone and inhibin have a negative feedback effect on the pituitary and hypothalamus
What is the role of progesterone in the menstrual cycle?
Progesterone stimulates the endometrium to become receptive to the implantation of a fertilised ovum
ALSO:
- negative feedback causing decreased LH and FSH (both needed to maintain the corpus luteum)
- an increase in the woman’s basal body temperature
What is the role of LH in the menstrual cycle?
causes the Graafian follicle to change into the corpus luteum, which begins to produce progesterone
What is the role of FSH in the menstrual cycle?
Stimulates the development of ovarian follicles at the begining of the menstrual cycle
The follicle most sensitive to FSH becomes the dominant Graafian follicle
How does pregnancy cause the cessation of menstruation?
If a woman becomes pregnant oestrogen and progesterone levels cause GnRH, FSH and LH to remain inhibited, thereby causing menstruation to cease
What are the phases of the menstrual cycle?
Follicular Phase (day 0-14) Ovulation (day 14) Luteal Phase (day 15-28)
Which follicle becomes the dominant one?
The one with the most FSH-receptors - becomes the most sensitive to FSH
When inhibin reduces release of FSH, the other follicles die (leaving just the dominant one)
What is the role of oestrogen in the menstrual cycle?
The Graafian follicle secretes increasing amounts of oestrogen to cause:
- endometrial thickening
- thinning of the cervical mucus to allow easier passage of sperm
- INHIBITION of LH production by the pituitary gland
Eventually oestrogen surpasses threshold level and STIMULATES LH production, resulting in a spike in LH levels around day 12
LH surge
~ day 12 of cycle
oestrogen surpasses threshold level and stimulates LH production
high amounts of LH cause the membrane of the Graafian follicle to become thinner.
Within 24-48 hours of the LH surge, the follicle ruptures releasing a secondary oocyte
The mature ovum is then released into the peritoneal space and is taken into the fallopian tube via fimbriae (finger-like projections)
Luteal Phase - no fertilisation
After ovulation, LH and FSH stimulate the remaining Graafian follicle to develop into the corpus luteum.
corpus luteum then begins to produce the hormone progesterone
As the levels of FSH and LH fall, the corpus luteum degenerates.
Degeneration of the corpus luteum results in loss of progesterone production.
The subsequent falling level of progesterone triggers menstruation and the entire cycle begins again
Luteal Phase - fertilisation
If an ovum is fertilised it produces hCG which is similar in function to LH.
hCG prevents degeneration of the corpus luteum (resulting in the continued production of progesterone).
Continued production of progesterone prevents menstruation.
The placenta eventually takes over the role of the corpus luteum (from 8 weeks gestation).
Two layers of endometrium
Functional layer: this grows thicker in response to oestrogen and is shed during menstruation
Basal layer: this forms the foundation from which the functional layer develops (i.e. it is not shed)
Phases of uterine cycle
Proliferative Phase
Secretory Phase
Menstrual Phase
Phases of uterine cycle - Proliferative
Driven by the endometrium being exposed to increasing levels of oestrogen
Oestrogen stimulates repair and growth of the functional endometrial layer allowing recovery from the recent menstruation (increasing endometrial thickness, vascularity and the number of secretory glands).
Phases of uterine cycle - Secretory
Begins once ovulation has occurred.
This phase is driven by progesterone
Results in the secretion of various substances by the endometrial glands, making the uterus a more welcoming environment for an embryo to implant.
Phases of uterine cycle - Menstrual
the corpus luteum degenerates (if no implantation occurs).
The loss of the corpus luteum results in decreased progesterone production.
The decreasing levels of progesterone cause the spiral arteries in the functional endometrium to contract.
The loss of blood supply causes the functional endometrium to become ischaemic and necrotic.
As a result, the functional endometrium is shed and exits through the vagina as menstruation.
Group I ovulation disorders
hypogonadotropic, hypogonadal anovulation
~10% of ovulation disorders
- Hypothalamic/pituitary failure.
- Low gonadotrophins and oestrogen deficiency
- E.g. brain surgery, eating disorders/reduced calories.
Group II ovulation disorders
normal gonadotrophins, normal oestrogen, problem within the ovary causing anovulation
~85% of women with ovulation disorders
Dysfunction of the hypothalamic-pituitary-ovarian axis.
Group III ovulation disorders
hypergonadotrophic, hypo-oestrogenic anovulation
~5% of ovulation disorders
Caused by ovarian failure
Parameters of “normal” menstrual cycle
24-38 days cycle length
≤ 7-9 days difference between shortest to longest cycles
≤ 8 days of bleeding
blood loss that does not interfere with a woman’s physical, social, emotional and/or quality of life.
Abnormal uterine bleeding
Absent/infrequent/frequent periods
Irregular cycle lengths
IMB, PCB, prolonged duration of bleeding
Heavy or light bleeding (subjective)
Heavy Menstrual Bleeding
= excessive menstrual blood loss (MBL) that interferes with the physical, social, emotional and/or material quality of life.
objective criteria of blood loss of >80 mL/cycle
Intermenstrual bleeding (IMB)
Bleeding between clearly defined cyclic and predictable menses
Postmenopausal bleeding (PMB)
Genital tract bleeding that recurs in a menopausal woman at least one year after cessation of cycles
= RED FLAG
Postcoital bleeding (PCB)
Non-menstrual genital tract bleeding immediately (or shortly after) intercourse
Chronic AUB
AUB has been present for the majority of the past 6 months
Acute AUB
Excessive AUB bleeding that requires immediate intervention to prevent further blood loss.
Amenorrhoea
Absence of uterine bleeding
How should Abnormal uterine bleeding (AUB) be described?
- regularity should be specified as irregular, regular or absent
- frequency should be specified as frequent, normal or infrequent
- duration should be specified as prolonged, normal or shortened
- volume should be specified as heavy, normal or light
Assessment of AUB
- Exclude pregnancy.
- Gynaecological history and examination.
=> Amount and timing of bleeding.
=> Signs of anaemia, palpation of masses, pelvic tenderness - Establish if chronic AUB (>6 months) or acute AUB (urgent intervention required).
- Use history to screen for coagulopathy.
- Investigations:
=> Full blood count (FBC), cervical smear, pelvic infection swabs and pelvic ultrasound (and coagulation screen if indicated).
=> TV USS – exclude masses/detect polyps - Referral to secondary care if malignancy is suspected.
Coagulopathy Screen for AUB
Structured history – positive screen if:
- Excessive menstrual bleeding since menarche, or
- One of the following:
- Postpartum haemorrhage,
- Surgery-related bleeding,
- Bleeding associated with dental work
• Two or more of the following:
- Bruising greater than 5 cm once or twice/month,
- Epistaxis once or twice/month,
- Frequent gum bleeding,
- Family history of bleeding symptoms
Gynaecological Red Flags
Suspected gynaecological cancer:
- Post-coital bleeding
- Post-menopausal bleeding
- Inter-menstrual bleeding
- Pelvic mass
- Cervix lesion
Causes of heavy menstrual bleeding (PALM-COEIN):
1. Structural: • Polyp (AUB-P) • Adenomyosis (AUB-A) • Leiomyoma (AUB-L) • Malignancy and Hyperplasia (AUB-M)
2. Non-structural: • Coagulopathy (AUB-C) • Ovulatory dysfunction (AUB-O) • Endometrial (AUB-E) • Iatrogenic (AUB-I) • Not yet classified (AUB-N)
Iatrogenic causes of AUB
exogenous sex steroid administration (combined oral contraceptives, progestins, tamoxifen),
intrauterine contraceptive device,
traumatic uterine perforation
Coagulopathy as cause of AUB
thrombocytopenia,
von Willebrand’s disease,
leukaemia,
warfarin
Ovulatory dysfunction as cause of AUB
PCOS, Congenital adrenal hyperplasia, Hypothyroidism, Cushing's disease, Hyperprolactinaemia
Treatment of HMB - first steps
All medical!
1st line - IUS
2nd line tranexamic acid/NSAIDs/COCP
3rd line - progesterones/GnRH
Why is IUS used first-line for treating HMB?
High rate of reducing HMB
generates more quality-adjusted life years than other medical treatments (tranexamic acid, NSAIDs, COCP) and at a lower cost
Treatment of HMB - further steps
Hysteroscopic/laparoscopic Myomectomy
Endometrial ablation
Resection of endometrium
Abdominal myomectomy
Hysterectomy
How does the Mirena-IUS work?
Intrauterine dose of 20 microgram/24 hours with little systemic absorption.
Inhibits endometrial proliferation, thickens cervical mucus and suppresses ovulation
What is the mirena-IUS licensed for?
Contraception, HMB, progesterone component of HRT
What are the requirements to be eligible for endometrial ablation?
Uterine cavity >10 cm length
No large fibroids/polyps distorting the cavity
No previous endometrial ablation
No active infective process
Myometrium is at least 10 mm if using the microwave ablation
Family is complete!
Why must the family be complete if a woman undergoes endometrial ablation?
Low chance of success of achieving pregnancy
If pregnancy achieved, high chance of miscarriage/infiltrating placenta.
Indications for hysterectomy for HMB
- Other treatment options have failed or are inappropriate
- Women have completed their families
- There is a wish for amenorrhoea
- Women (who have been fully counselled) request it or other forms of further treatment are contraindicated.
Types of hysterectomy
- Abdominal hysterectomy (AH)
- Vaginal hysterectomy (VH)
- Laparoscopic-assisted vaginal hysterectomy (LAVH).
- Total laparoscopic hysterectomy (TLH)
- Subtotal hysterectomy (STH)
Causes of IMB
- Ovarian: 1-2% ovulation spotting, oestrogen secreting tumours
- Uterine: iatrogenic (contraception), infection, structural benign or malignant
- Cervical: iatrogenic (examination, smear), infective, structural benign or malignant
- Vaginal: infective, structural benign or malignant
Management of IMB
Medical:
- IUS/COCP
- Progesterones
- HRT (if irregular bleeding during menopause)
Surgical – same as for HMB, but ablation is less effective.
Dysmenorrhoea
= painful periods
High prostaglandin levels cause painful uterine contractions and ischaemia
classified as primary or secondary
Primary dysmenorrhoea
Occurs with the start of menstruation
No organic cause
Tx: NSAIDs, COCP
Secondary dysmenorrhoea
Precedes and relieved by menstruation
Caused by pelvic pathology
=> fibroids, adenomyosis, endometriosis, PID, malignancy
Ix – pelvic USS, hysteroscopy
Tx depends on cause
Post-coital bleeding
= Vaginal bleeding after intercourse that is not menstrual loss.
Always abnormal (unless 1st intercourse)
ALWAYS exclude cervical cancer
Causes of post-coital bleeding
Cervical carcinoma – MUST EXCLUDE
=> Cervical inspection and smear.
=> If no obvious cause, colposcopy to exclude malignancy.
Cervical ectropions/eversion
Benign cervical polyps
Hypertension at booking visit
NOT pre-eclampsia
=> Essential or secondary HTN
Need:
• Careful history & physical examination
• U&Es
• Urine microscopy/renal USS/urinary catecholamines
When does pre-eclampsia occur?
After 20 week’s gestation
What is pre-eclampsia?
= an endothelial cell disorder involving an excessive inflammatory response to pregnancy
it is CAUSED by pregnancy and CURED by delivery (of the placenta)
What are the features of pre-eclampsia?
Hypertension
Proteinuria
Oedema
Multiorgan involvement
Foetal compromise
Significant maternal morbidity
What are risk factors for pre-eclampsia?
- Extremes of reproductive age
- Socio-economic status
- Ethnic groups
- Genetic factors
- Multiple pregnancy
- Primigravida
- Assisted conception
- Previous pre-eclampsia
- Obesity
- Chronic renal disease
- Chronic hypertension
- DM
- Connective tissue diseases
- Certain thrombophilias
Pathophysiology of pre-eclampsia
- Abnormal Placentation
- Endothelial Cell Dysfunction
- Organ Hypoperfusion
- Plasma Volume Loss
Pre-Eclampsia - abnormal placentation
- Failure of invasion of trophoblast cells
- Maternal spiral arteries continue to have thick muscular walls
- Reduced maternal perfusion of placenta and possible vasospasm
- Placental damage leading to increased apoptosis (cell death)
- Release of circulating factors or placental syncytial fragments
Pre-Eclampsia - Endothelial Cell Dysfunction
- Tissue oedema (increased endothelial cell permeability)
- Hypertension (altered production of vasodilator substances)
- Clotting dysfunction (abnormal production of procoagulants by endothelial cells)
Pre-Eclampsia - Organ Hypoperfusion
- Due to chronic/acute vasoconstriction
* Underperfusion/focal ischaemia in kidneys, liver, brain
Pre-Eclampsia - Plasma Volume Loss
- Intravascular compartment becomes constricted and underfilled.
- May be considerable tissue oedema
- Low intravascular volume contributes to poor organ perfusion (including of the fetoplacental unit)
Foetal complications of pre-eclampsia
IUGR Intrauterine hypoxia Prematurity Increased risk of placental abruption Stillbirth/intrauterine death HTN/IHD/metabolic disease later in life
Maternal complications of pre-eclampsia
Eclampsia - Grand mal seizures due to cerebral vasospasm
Cerebrovascular Haemorrhage Retinal detachment DIC Thromboelbolism Renal failure Pulmonary oedema HELLP Syndrome (liver failure)
HELLP syndrome
H - Haemolysis (low grade, rarely enough to cause severe anaemia)
EL - Elevated liver enzymes (transaminases, lactate dehydrogenases, bilirubin)
LP – Low platelets
What is used for treatment of eclamptic seizures?
Mg Sulphate
Umbilical artery - absent end diastolic flow
can be normal in early pregnancy (up to 16 weeks)
mid to late pregnancy it usually occurs as a result of placental insufficiency
Umbilical artery - reduced end diastolic flow
Indicates significant increase in resistance to blood flow within the placenta
Associated with significant perinatal mortality
Indications for delivery in Pre-eclampsia
Hypertension remaining uncontrolled despite maximal antihypertensives
Eclampsia
Renal, hepatic or coagulation impairment
Pulmonary oedema
Foetal distress
Milder pre-eclampsia at term
Which antihypertensive medications are used in pregnancy?
Labetalol Nifedipine Methyldopa Prazosin/Doxazocin Atenolol
Hydralazine in emergencies
Which antihypertensive medications are avoided in pregnancy?
ACEis and diuretics
Involution of the Uterus
= Return of the uterus to pre-pregnant size
Normally firm and in midline
Fundus at the level of the umbilicus post-partum Day 1
Descends one finger breadth (1 cm) a day for 10 days
What are possible post-partum problems?
PPH (primary or secondary) Haematoma Infection VTE Mood disturbance
Symptoms of post-partum haematoma
Severe pain Mass felt on vaginal examination Flank pain Abdominal distension Shock
Management of post-partum haematoma
Conservative (if small)
Surgery – incision and drainage
Vaginal pack
Catheter
Puerperal infection
= infection of the genital tract that occurs at any time between the onset of rupture of the membranes or labour and the 42nd day post-partum (or post-termination).
Predisposing factors for puerperal infection
Poor nutrition Low socio-economic group Hx of infections Anaemia Immunodeficiency
Prolonged labour PROM Poor aseptic technique Birth trauma / Episiotomy Multiple VEs C-section
Manual removal of placenta
Haemorrhage
Retained products
Endometritis
= infection of the uterus (endometrium, myometrium, or parametrium)
Ascends from lower genital tract
usually occurs within 10 days of delivery/miscarriage/termination
Risk factors for post-partum endometritis?
Most important factor is mode of delivery
=> 1-3 % risk after NVD, 15-40% after Caesarean section
Also:
PROM, multiple vaginal examinations, UTI, GBS carrier, DM, poor nutrition, poor health, catheterisation
Signs and symptoms of endometritis
Fever, abdominal pain, offensive discharge
Pyrexia, tachycardia, lower abdominal tenderness, offensive discharge, uterine and adnexal tenderness
Endometritis - investigations
Bloods – FBC, CRP, (+/- U&E, coagulation)
Cultures – bloods, swabs (+/- MSU)
Endometritis - management
Antibiotics (broad spectrum)
Analgesia
Drain any collection
Consider Sepsis 6 bundle (blood cultures, IV Abx, fluid, serum lactate, oxygen, catheter)
What is mastitis?
When does it develop post-partum?
= Infection of breast tissue
Develops after breast milk is established, 2-4 weeks postpartum
Causes of mastitis
Bacteria enters through cracks in nipple Milk stasis Poor hand washing Breast not dry or wet breast pad Incorrect placement of baby causes sore nipples
Risk factors for mastitis
ineffective or infrequent breast feeding or milk stasis from engorgement, skipping a breast
What are common pathogens causing mastitis?
E. Coli or Staph. aureus
Signs and symptoms of mastitis
Fever, chills, malaise, painful, warm, red area of breast
Management of mastitis
Supportive bra
Breast feed frequently
Warm compress before feeding
Cold packs between feedings
Analgesia
Antibiotics (flucloxacillin or erythromycin)
Increase fluids
Drain any abscess
Post-partum UTI
Bladder hypotonia post-delivery and residual urine and reflux leads to increased risk of UTI
Most commonly caused by E. coli
Risk factors for post-partum UTI
Frequent VE, catheterisation, birth trauma
Sites of Post-partum Wound Infection
Incision (Caesarean),
Perineum (episiotomy or laceration)
Signs and symptoms of wound infection
Erythema, bruising, oedema, purulent drainage, wound edges not approximated, pain, tenderness, pyrexia and signs of sepsis
Management of wound infection
Wound and blood cultures Sutures/staple removal Antibiotics (broad spectrum) Analgesics Wound dressing (involve specialists) Drain purulent material Surgery
Sepsis bundle if necessary
Causes of VTE in pregnancy?
Hypercoagulability of blood (↑ factor VIII, IX, X thrombin),(↓ fibrinolytic activity protein S)
Venous stasis
Endothelial injury
Prevention of VTE
Avoid dehydration Avoid trauma to legs (lithotomy) Early postpartum mobilisation Leg exercises to support venous return Avoid smoking TED stockings
Prophylactic anticoagulants
RCOG VTE assessment tool
what is a Positive Homan’s sign ?
What might it indicate?
pain in the calf is produced by passive dorsiflexion of the foot
indicates possible DVT
Diagnosis of DVT
Doppler USS
Treatment of CVT
LMWH (start before diagnosis confirmed)
(+/- warfarin in the post-natal period).
=> Duration: 3 months
Elevate leg and TEDS
Symptoms/signs of PE
- Sudden, sharp, pleuritic chest pain
- Shortness of breath/tachypnoea
- Cough/Haemoptysis
- Tachycardia
- Sweating
- Pyrexia
- Hypotension/Collapse
Investigations for suspected PE
- Blood gases: hypoxia
- CXR
- ECG
- V/Q scan
- CTPA
- Leg Doppler if symptomatic
Management of PE
= MEDICAL EMERGENCY
- Anticoagulation (LMWH) prior to confirming diagnosis
- Analgesia
- Oxygen
- (Thrombolysis / Embolectomy)
Any woman with VTE in pregnancy/puerperium will require AN and PN thromboprophylaxis in subsequent pregnancies.
Baby blues
~70% of women (very common)
Occurs a few days after birth (day 3-4 PN), but self-limiting (days, up to 2 weeks)
Transient feelings of tearfulness, fatigue, anxiety and irritability; Mild depression with interspersed happier feelings
No association with previous psychiatric history.
Postnatal Depression - onset
Onset between birth and 1 year post-natal
Highest risk in first 3 months
how common is Postnatal Depression?
Common – 10-15% of women
Risk factors for post-natal depression
• Primiparity
- Personal history of depression or substance misuse.
- Depression during pregnancy
- Family history of depression
- Lack of support/ single parent
- Marital or financial stress
- Birth complications
- Pre-term birth
DDx for post-natal depression
puerperal psychosis, postpartum thyroiditis, anaemia
Treatment of post-natal depression
Medication – SSRI
Counselling/cognitive therapy
Support groups
How common is Puerperal Psychosis?
When does it normally occur?
Less common: 0.1 - 0.2% of births
Usually occurs 3-6 weeks after delivery (up to 1 year)
Who is at highest risk of puerperal psychosis?
People with:
- bipolar disorder,
- previous puerperal psychosis
- schizo-affective disorder
Symptoms of puerperal psychosis
Symptoms of depression
In addition, there can be:
- Agitation
- Restlessness
- Obsessive thoughts about baby
- Rapid mood swings (mimic bipolar)
- Delusions/ Hallucinations
- Paranoia
- Suicidal or homicidal thoughts
Treatment of puerperal psychosis
= Medical emergency (suicide/infanticide risk)
Hospitalisation (psychiatric mother and baby unit: voluntary or under MHA)
Antipsychotic medication
Psychotherapy
Hormonal control of spermatogenesis
LH causes testosterone production in Leydig cells
Testosterone and FSH control synthesis and transport of sperm in Sertoli cells
Definition of infertility
= the inability to conceive after 1-year unprotected vaginal sexual intercourse, without any known cause of subfertility in a woman of reproductive age.
How many couples will conceive within 1 year of trying?
~80%
What is the impact of infertility?
Sense of failure Marital disharmony Psychological illness Financial implications – IVF treatment Anxieties – can continue during pregnancy, if it is achieved.
Potential Causes of Subfertility
- Unexplained
=> A large proportion occur due to defective implantation. - Male factors
- Ovulation dysfunction
- Tubal damage
- Endometriosis
- Coital problems
- Cervical factor
What are the possible causes of male infertility?
Primary Testicular Failure
Hypogonadotrophic (Secondary Testicular Failure)
Androgen Resistance (Testicular Feminisation)
Genital Tract Obstruction - CF, absence of vas deferens, chlamydia/gonnorhoea
Immotile Sperm Problem with Coitus Uncertain Aetiology Systemic Illness Lifestyle Factors
What are lifestyle factors that can affect fertility?
Drugs/ toxins – Therapeutic, occupational, recreational
Smoking Alcohol intake Caffeine Weight Stress/sleep dysfunction
How can sleep disturbances/stress affect male fertility?
Testosterone secretion follows a diurnal pattern and increased with REM sleep.
What are causes of Primary Testicular Failure?
Congenital - e.g. Klinefelter’s
Acquired - e.g. Mumps orchitis, testicular torsion, trauma, inguinal/scrotal surgery, radiotherapy
Causes of Secondary Testicular Failure?
Idiopathic
Acquired - e.g. cranial space occupying lesions, trauma, meningitis
What are causes of female infertility?
Anovulation Thyroid Dysfunction Tubal Damage Uterine Problems Cervical Problems
Increasing age Lifestyle factors Implantation defects Embryo development issues Metabolic disorders, immunological and genetic factors
Causes of anovulation
- PCOS
- Hyperprolactinaemia
- Hypothalamic Hypogonadism
- Premature ovarian failure
Sx of PCOS
infertility,
oligomenorrhoea,
hirsutism
Risk factors for PCOS
genetics,
high BMI,
T2DM
what occurs in Hypothalamic Hypogonadism in women?
What causes it?
Decreased GnRH release = decreased LH/FSH and oestrogen.
Causes – anorexia nervosa/reduced BMI, athletes, stress, Kallman Syndrome
Kallmann syndrome
lack of production of certain hormones that direct sexual development
Causes delayed or absent puberty and an impaired sense of smell
How does hyperprolactinaemia cause anovulation?
Increased prolactin causes decreased release of GnRH
What can cause tubal damage?
- Infection - PID, STIs
- Endometriosis
- Previous Pelvic Surgery
What uterine problems can affect fertility?
Submucous fibroids
Intrauterine adhesions
Polyps
Anatomical abnormalities
What Cervical Problems can affect fertility?
Cervical mucous hostility/anti-sperm antibodies
=> Kills sperm
Loop excision of TZ of cervix.
=> No mucous for sperm to travel in
What investigations are done for male infertility?
Semen Analysis
Sperm DNA Fragmentation Test
Blood tests – FSH, LH, TSH, testosterone, prolactin
Testicular examination
Genetic – Karyotype, CF screening
How is semen analysis performed?
Sample produced by masturbation after 2-7 days abstinence
Analysed within 1-2 hours, repeat abnormal results in 12 weeks
Values measured = Volume, Total sperm, Sperm conc., Total motility, Morphology, Vitality, pH
What is the normal volume of ejaculate?
> 1.5 mL
What is a normal sperm count?
> 15 million/mL
Azoospermia
= no sperm in ejaculate
Oligospermia
= low sperm count in ejaculate
<15 million/mL, severe if <5 million/mL
Asthenospermia
= sperm count where motility is poor.
What investigations are done for female infertility?
Rubella Status Cervical swabs Follicular Phase Hormone Profile Endocrine Profile (if indicated) Ovulation Detection Tests of tubal latency USS scan of anatomy
Follicular Phase Hormone Profile
Day 1-5 if regular periods, any time if irregular/absent
Measure FSH, LH, oestradiol
Follicular phase - FSH levels
- FSH raised in ovarian failure
- FSH low in hypothalamic failure
- FSH normal in PCOS
Ovulation Detection
Luteal progesterone
=> day 21 should be mid-luteal increase (if 28-day cycle)
USS ovulation tracking to detect follicle size/rupture
Basal Body temperature
Management of male infertility
Lifestyle changes:
- Reduce or stop smoking/alcohol/drug exposure
- Weight management
- Testicles below body temperature (loose clothing/cooling methods).
Hormonal – gonadotrophins
Varicocoele – surgery
Intrauterine Insemination with donor/husband semen
Assisted contraception techniques
Management of female infertility
General Measures:
- Folic acid/Vitamin D
- Diet and weight advice
- Reduce or stop smoking/alcohol/drug exposure
- Cervical smear
Ovulation Induction
Assisted contraception techniques
What is the 1st line for Ovulation Induction?
How does it work?
Clomifene - used for ~6-9 cycles
Acts to decrease oestrogen levels, so the brain releases more GnRH => More FSH, LH for follicle development.
What are other mechanisms (apart from clomifene) to induce ovulation ?
Gonadotrophins
Metformin (insulin sensitisation in PCOS, often used combined with clomifene)
Letrozole (aromatase inhibitor)
Laparoscopic ovarian drilling
Dopamine agonists (for hyperprolactinaemia)
Risks of ovulation induction
If >1 follicle develops, there is risk of multiple pregnancies
Ovarian Hyperstimulation syndrome (OHSS)
what is Ovarian Hyperstimulation syndrome (OHSS)?
Exposure of hyperstimulated ovaries to hCG leads to the production of pro-inflammatory mediators
increased vascular permeability leads to loss of fluid into the third space
Sx – abdominal discomfort/pain (+/- oedema, ascites, SoB, hypovolaemia)
RFs - gonadotrophins, IVF, <35yo, PCOS
Management is supportive treatment
Indications for assisted conception:
- All other methods have failed
- Male factor subfertility
- Unexplained subfertility >2 years
- Endometriosis/tubal blockage
- Genetic disorders
Intrauterine Insemination
15-20% success
Insert sperm into uterus (often following ovarian stimulation)
Cheaper than IVF but need patent fallopian tubes
Useful if cervical factors/endometriosis
In Vitro fertilisation
35% success per cycle (10% if >40 years old)
Consider after 2 years of trying to conceive
Sperm and oocyte mixed in petri dish
Needs normal oocyte production (not possible in ovarian failure)
Pre-implantation genetic diagnosis if >37yo mother/high risk of genetic conditions
Steps of IVF
- Follicular development
- Ovulation induction
- Egg collection (transvaginal aspiration with USS guidance)
- Fertilisation and transfer
Risks of IVF
haemorrhage on egg collection, failure, multiple pregnancy, OHSS, ectopic pregnancy
Why is cardiac disease a major cause of maternal mortality during pregnancy?
what are important symptoms?
a damaged heart copes less well with the increased demand during pregnancy.
It is often difficult to differentiate pathological cardiac symptoms from physiological ones in pregnancy
=> Persistent tachycardia and orthopnoea are important and should be fully investigated
When does maternal cardiac disease cause the most problems in pregnancy?
> 28 weeks
OR
During labour:
- 1st stage – sympathetic response to pain and anxiety, supine position.
- 2nd stage – BP increases with pushing, venous return decreases with pushing.
- 3rd stage – up to 1L of blood returns to circulation
Management of pregnancy with maternal cardiac disease
Consultant-led care
Treat conditions before pregnancy if possible.
Review medications and stop contraindicated drugs (e.g. warfarin, ACEI)
Regular checks – BP, anaemia, foetal abnormalities
Management of labour/birth with maternal cardiac disease
- CTG monitoring
- Epidural (Pain control and reduces maternal tachycardia)
- Position – avoid supine
- Vaginal birth is recommended, unless obstetric indications for C-section (Less rapid haemodynamic changes)
- Depending on severity, pushing (active 2nd stage) may be avoided and forceps/ventouse used to facilitate delivery.
Problems associated with epilepsy in pregnancy
Seizure control is decreased (especially in labour or when sleep deprived)
Morning sickness can affect medication
Seizures can be associated with foetal hypoxia.
Recurrent tonic-clonic seizures can cause IUGR
There is increased risk of NTDs and also congenital heart defects, urinary tract/skeletal abnormalities and cleft palate due to medication
Antenatal management of epilepsy in pregnancy
Consultant-led care
Seizure control (aim for seizure free)
=> As few drugs as possible, at the lowest dose.
=> Involve the neurology team – DO NOT change drugs without their advice.
=> Sodium valproate is contraindicated unless no alternative therapies.
=> Safest drugs – carbamazepine, lamotrigine
Folic acid supplementation – 5mg OD pre-conception
Vitamin K supplementation – 10mg OD from 36 weeks
Offer high resolution USS for anomalies (18-20 weeks) and serial growth scans
Intrapartum management of epilepsy in pregnancy
Hospital delivery
Continue AEDs during labour
Appropriate care/analgesia to minimise risk factors for seizures (such as insomnia, stress and dehydration).
=> But avoid pethidine, as it increases seizure frequency.
Postnatal management of epilepsy in pregnancy
Continue AEDs (may require dose adjustment)
Support to minimise triggers for seizures (sleep deprivation, stress, pain)
Safety strategies for minimising risk to baby during seizures
Contraception – will depend on which AEDs the patient is taking.
Obesity - maternal risks
Thromboembolism Pre-eclampsia GDM C-section PPH Wound infection Epidural failure/aspiration during GA Difficult IV access
Obesity - foetal risks
Congenital abnormalities Increased mortality Miscarriage/stillbirth NTDs Macrosomia (causing shoulder dystocia)
Antenatal management of maternal obesity
Lifestyle advice – diet, exercise, weight loss
Consultant-led care
5mg folic acid and VitD
Thromboprophylaxis
Monitor for GDM and HTN
=> OGTT at 28 weeks
=> Serial growth scans
Intrapartum/Postnatal management of maternal obesity
IOL if large baby Continuous CTG in labour May need to use FSE if difficult contact with CTG Thromboprophylaxis Active management of 3rd stage
Glycaemic changes in pregnancy
- Increased peripheral resistance to insulin due to hormones
=> Higher post-prandial glucose
=> Resistance increases with gestation. - Transplacental glucose transport to the foetus – lowers fasting glucose.
=> Reflects maternal levels (hyperglycaemia means more transported to foetus)
Complications of Hyperglycaemia in Pregnancy
= Related to glucose levels, so usually less severe in GDM.
MATERNAL: Hypoglycaemia/ketoacidosis Infection Pre-eclampsia Deterioration of pre-existing disease (e.g. retinopathy/nephropathy)
FOETAL: Hypoglycaemia Respiratory distress syndrome Congenital abnormalities (glucose = teratogenic) IUGR/IUFD Macrosomia Polyhydramnios Preterm labour Stillbirth Birth complications
How can maternal hyperglycaemia cause foetal macrosomia?
High maternal blood glucose crosses the placenta and stimulates foetal insulin production, which acts as a growth promotor (bone, muscle, adipose).
Management of pre-existing DM in pregnancy
Pre-pregnancy:
- Optimise glycaemic control
- Folic acid 5mg OD
During pregnancy:
- Increase insulin dose to maintain normoglycaemia
- Aspirin 75mg daily to reduce pre-eclampsia risk
- Regular BM, HbA1c, BP and renal monitoring.
- Regular foetal monitoring (20-week USS and regular growth scans)
Delivery by 39 weeks.
What is GDM?
What causes it?
= Glucose intolerance first diagnosed in pregnancy (may or may not resolve after).
occurs if pancreatic beta-cells are unable to produce sufficient insulin to counteract the normal glycaemic changes in pregnancy
Risk factors for GDM
PMHx/FHx of GDM 1st degree relative with DM BMI >30 Ethnicity (Black Caribbean, south Asian) Previous large foetus (>4.5kg) Previous unexplained stillbirth
Screening for GDM
Booking appointment – screen for risk factors
28 weeks if RFs (or ASAP if previous GDM/DM) – OGTT
OGTT any time if detect pregnancy risk factors (polyhydramnios, persistent glucosuria)
Antenatal Management of GDM
- Lifestyle advice – diet and exercise
- Oral agents – e.g. metformin
- Insulin
- 75mg aspirin (prophylaxis for pre-eclampsia)
- Folic acid 5mg
- Regular foetal growth scans
- Further Ix:
- HbA1c (rule out T2DM)
- Abdominal palpation (SFH, lie, pain)
- USS & foetal artery dopplers
Post-partum management of GDM
Educate on increased lifetime risk of DM
Educate on increased recurrence of GDM
Carefully monitor foetus for 24 hours
What is menopause?
= the permanent cessation of menstruation due to loss of ovarian activity after the natural depletion of oocytes
Perimenopause
= from first onset of symptoms to 12 months after last menstrual period.
Post-menopause
= the period after 12 months since last menstrual period
What is the average age of menopause?
When is menopause considered premature?
= 51 years
= menopause before 40 years old
How is menopause diagnosed?
If healthy and >45, diagnosis is based on vasomotor symptoms and irregular periods.
If <45, then blood tests to measure FSH are required for diagnosis.
Symptoms of menopause
Vasomotor symptoms – hot flushes and night sweats
Urinary problems – frequency, urgency, nocturia, incontinence, infection.
Vaginal atrophy – dyspareunia, itching, burning, dryness
Loss of libido
Psychological symptoms (e.g. anxiety/depression, reduced concentration, mood swings, forgetfulness)
Risk of CVD
Risk of osteoporosis (fractures)
Menopause - what investigations may be needed?
- Check ovarian reserve - FSH levels
- Rule out other causes of symptoms (TSH, catecholamines)
- DEXA scan to check for osteoporosis/fracture risk
- Investigations to check suitability for HRT
What will FSH levels be during the menopause?
raised due to loss of -ve feedback from oestrogen
What is a pre-requisite for oestrogen-only HRT for the menopause?
Patient must not have a uterus (risk of endometrial ca)
Menopause - Benefits of HRT
Treats vasomotor, vaginal and urinary symptoms
Reduces risk of osteoporosis and fractures
Reduces risk of colorectal cancer
Prevents dementia and preserve cognition
Menopause - Risks of HRT
Oestrogen only – endometrial cancer
Combination – breast cancer
Increased risk of VTE/CVA
Increased risk of gallbladder disease
Side effects of HRT
Headaches, nausea, Mood swings, Abnormal PV bleeds, Fluid retention, breast tenderness, Dyspepsia.
How long is HRT provided for the menopause?
5 years at the lowest effective dose, and then review the risk vs. benefit.
What type of HRT regime is used for perimenopausal women?
CYCLICAL combined HRT
= daily oestrogen and 14 days of progesterone (either monthly or 3-monthly, to induce bleed).
What type of HRT regime is used for postmenopausal women?
CONTINUOUS combined HRT
= daily oestrogen and progesterone (amenorrhoea)
What non-HRT options are available for managing symptoms of menopause?
Lifestyle measures – meditation, stop smoking, reduce alcohol intake, exercise.
Hot flushes/night sweats – SSRIs, clonidine
Vaginal atrophy – lubricants, creams, moisturisers
Osteoporosis – lifestyle factors, bisphosphonates, calcium/vitD, raloxifene, denosumab
What is a normal Symphysial Fundal Height ?
Normal = gestation +/- 2cm
Not usually measured before ~20 weeks
What may make SFH inaccurate?
BMI >35
Large fibroids
Polyhydramnios
what should women be offered if foetal AC or EFW is <10th centile, or there is evidence of reduced growth velocity?
women should be offered serial assessment of fetal size and umbilical artery Doppler
Symmetrical SGA
= small HC and AC,
occurs from early pregnancy
~20% of SGA cases
Asymmetrical SGA
= normal HC, small AC
occurs later in pregnancy
~80% of SGA cases
Small for gestational age (SGA)
= a statistical observation
Definitions vary – generally foetus <10th centile for gestational age (WHO)
When can SGA be normal?
Can be constitutionally small – no pathology is present.
=> Contributing factors include ethnicity, sex, and parental height.
Foetal Growth Restriction (FGR)
= Failure of foetus to reach its genetic growth potential – due to a pathological process.
Growth velocity slows down or stops because of inadequate nutrition supply and utilisation and/or oxygenation
Causes of FGR - placenta-mediated
- Utero-placental insufficency
- Pre-eclampsia
Causes of FGR - non-placenta mediated
- Chromosomal abnormality
- Congenital anomaly
- An error in metabolism
- Foetal infection – varicella, CMV, rubella, syphylis, toxoplasmosis, (malaria)
Maternal factors:
- Nutrition
- Smoking, Alcohol
- Drugs – cocaine, heroin, beta-blockers.
- Maternal disease
What determines how many growth scans a woman will have during pregnancy?
Women with 1 major risk factor – serial growth scans
Women with ≥3 minor risk factors – uterine artery doppler at 20-24 weeks to decide if additional scans warranted and how frequently
Prevention of FGR
Aspirin (small effect - increase placental blood flow)
Stop smoking
Management of FGR
Optimal surveillance method and frequency:
- Foetal biometry and amniotic fluid volume
- Umbilical artery Doppler +/- regional Dopplers
- Foetal medicine surveillance may be recommended
Timing of delivery = dependent on doppler results.
- Caesarean if abnormal umbilical Doppler (AEDF/REDF)
- Steroids to promote lung development if pre-term delivery.
- Continuous monitoring in labour
- Neonatologist at delivery
Foetal Macrosomia
(also LGA)
= EBW >90th centile for gestational age
= Birth weight > 4000g or 4500g
Risk factors for foetal macrosomia
Previous macrosomia
Foetal sex (male) Genetic factors - taller, heavier patients tend to have larger babies
Maternal diabetes / Obesity
Excessive maternal weight gain
Post-dates pregnancy
Multiparity
Congenital anomalies (hydrops)
Genetic disorders (e.g. Beckwith-Wiedermann)
What labour/post-partum complications can occur due to macrosomia?
- Prolonged first stage of labour => need for augmentation
- Prolonged second stage of labour => need for instrumental delivery
- Shoulder dystocia and birth trauma (nerve damage, fractures, birth asphyxia)
- Emergency caesarean section
- Perineal trauma
- Post-partum haemorrhage
- Neonatal hypoglycaemia
What are the available options for unwanted pregnancy?
- Continuation of pregnancy
- Continuation and offer for adoption/fostering
- Termination of pregnancy (not available in all countries!)
Grounds for termination of pregnancy?
A. The continuation of pregnancy would involve risk to the life of the pregnant woman greater than if the pregnancy were terminated.
B. The termination is necessary to prevent grave permanent injury to the physical/mental health of the pregnant woman.
C. The pregnancy has not exceeded its 24th week and the continuation of pregnancy would involve risk greater than if the pregnancy were terminated to the physical/mental health of the pregnant woman.
D. The pregnancy has not exceeded its 24th week and that the continuation of pregnancy would involve risk greater than if the pregnancy was terminated to the physical/mental health of any existing children or the family of the pregnant woman.
E. There is substantial risk that if the child were born it would suffer from such physical/mental abnormalities as to be seriously disabled.
What is the most common ground for terminating a pregnancy?
C is the most common ground for termination, followed by E.
ToP in under 16s
Explain limits of confidentiality – assess Gillick Competency/Fraser Guidelines
Safeguarding assessment
Explore support available
<13s unable to consent to sex = MUST refer to social care
Referral to TOP
- Self-referral by contacting an abortion provider directly
- GP referral to an abortion service
- Sexual health clinic can redirect to abortion provider
Medical TOP - drugs used
- Mifepristone (Antiprogesterone)
• Dose = 200mg orally
• Interrupts the pregnancy by encouraging placental detachment.
• Induces cervical ripening and uterine contractions - Misoprostol (Prostaglandin):
• 24-48 hours after Mifepristone.
• 1st Dose = 800mcg vaginally (can be done at home)
• 2nd dose = 400mcg vaginally/orally after 4 hours.
• Repeated dosage used 3 hourly for late MTOP
• Uterotonic effects cause softening of the cervix and contraction of the uterus, causing expulsion of the products of conception.
Timings of MTOP
Early MTOP = before 10 weeks.
Late MTOP = after 14 weeks
(Between 10-14 weeks, surgical TOP is required)
If >22 weeks, inject foetal heart/umbilical cord with KCl to prevent live birth.
Contraindications to MTOP
- Pulmonary HTN
- Oral Steroid use
- Bleeding disorder/anticoagulant use
- Renal insufficiency
- Severe asthma
- Previous CVA
- Breastfeeding
- Anaemia
Surgical TOP
Give pre-op Abx to cover against chlamydia and anaerobes.
Tends not to be used before 10 weeks (medical methods used).
Misoprostol can be given for cervical ripening before surgical TOP.
- 7-13 weeks – suction curettage TOP (under GA or LA)
- > 13 weeks – surgical TOP by dilatation and evacuation.
Side effects of TOP
- Dizziness, hot flushes
- Diarrhoea and nausea
- Period-like cramping
- Vaginal bleeding
Complications of MTOP
- Haemorrhage
- Infection (10%)
- Failure (1%)
Complications of surgical TOP
- Haemorrhage
- Infection (10%)
- Uterine perforation
- Cervical trauma
- Risk of preterm delivery
- Failure (0.2%)
What is the impact of abortion on future pregnancies ?
Abortion does not affect future fertility
Post-termination care
Analgesia and 24-hour support helpline.
Anti-D immunoglobulin to all non-sensitised Rh-negative women
ABX prophylaxis
Follow up after MTOP – rule out ongoing pregnancy/ectopic.
=> low sensitivity pregnancy test 2-3 weeks after medical TOP.
TOP and retained products of conception
Hx of prolonged bleeding and pain
Bulky, soft uterus with open cervical os = clinical diagnosis
USS to r/o live pregnancy
Pregnancy test can remain positive for up to 6 weeks and is not diagnostic.
Managed expectantly, medically or surgically
What are forms of LARC?
Implant
IUS
IUD
Injection
What is the main action of the Progestogen Releasing Implant
Mainly prevents ovulation
Also thickens mucous and thins endometrium
Implant - insertion
Time to effect = 7 days (use barrier contraception for 7 days).
Inserted sub-dermally, over the triceps muscle (under local anaesthetic)
How long is the contraceptive implant licensed for?
3 years
Implant - Cautions/Contraindications
current breast cancer, past breast cancer, CV event while using method, liver conditions.
Implant - Advantages
Immediate return to fertility on removal
Compliance not an issue
Implant - Side effects
Hormonal related – irregular bleeding/amenorrhoea, headaches, mood, breast tenderness
Procedural risks – bruising, infection at site, etc
Copper IUD - mechanism of action
Acts by blocking fertilisation (toxic to sperm).
As emergency contraception, it prevents implantation
What must be excluded before insertion of IUD/IUS?
MUST exclude pregnancy
also STI
IUD - advantages
- Time to effect = instant (immediate protection).
- Unaffected by D&V
- Rapid return to fertility
IUD - contraindications/cautions
- Unexplained HMB
- Previous ectopic
- Gestational trophoblastic disease
- Cervical/endometrial cancer.
- Active/recent pelvic infection
IUD - side effects
- Periods may be heavier, longer and more painful (but usually settles)
- Risks associated with insertion – pain, bleeding, infection
- Perforation of uterus
- Can fall out (counsel to check threads after every period).
- Ectopic pregnancy
IUS - mode of action
prevents fertilisation and implantation
How long does an IUD or IUS take to work?
IUD - instant effect
IUS - 7 days to effect
IUS - advantages
- Lighter, less painful periods (Mirena is only IUD licenced for HMB)
- Less hormonal SEs as actions more localised
- Unaffected by D&V
- Rapid return to fertility.
IUS - contraindications/cautions
The same as IUD, but also breast cancer
IUS - side effects/risks
- Irregular bleeding for 3-6 months
- Hormonal-related effects – headaches, mood changes, breast changes.
- Procedural risks
- Perforation
- Can fall out
- Ectopic pregnancy
Contraceptive injection - Mode of action
Prevents ovulation, also thickens mucous and thins endometrium
Contraceptive injection - length to effect
7 days to take effect
Why is the typical use failure rate for the contraceptive injection higher than other LARCs?
6% with typical use, 0.2% with perfect use
Relies on coming back for the injection every 12 weeks.
Contraceptive injection - contraindications/cautions
Current breast cancer, osteoporosis risk, obesity
Contraceptive injection - advantages
- May have less painful, lighter periods.
- Unaffected by D&V
Contraceptive injection - side effects/risks
- Delay in return to fertility
- Reversible effect on bone density
Also: Hormonal side effects Weight gain Irregular bleeding/amenorrhoea Cannot be removed
COC - mechanism of action
Mainly inhibit ovulation,
Also thickens cervical mucous, thins endometrium
How is the COC taken?
3 weeks on and 1 week off, or back-to-back.
Effectiveness of COC?
- Perfect use – failure rate 0.3%
- Typical use – failure rate 8%
Time to effect = 7 days
COC - advantages
- Lighter and less painful periods.
- Protective against endometrial, ovarian and bowel cancers.
- Protective against fibroids, ovarian cysts, endometriosis
COC - side effects/risks
- Nausea, headaches, dizziness
- Decreased libido
- Breast tenderness
- VTE, MI/CVD, CVA, migraine
- HTN
- Breast/cervical cancer
COCP - contraindications/cautions
- VTE, CVA, IHD
- Migraine with aura
- Breast/endometrial cancer
- BMI >40
- Pregnancy
- > 40 years old (>35 if smoker)
COC - missed pills
- If D&V within 2 hours of taking the pill, take another.
- >2 missed pills = 7 days condom use
POP - mechanism of action
inhibit ovulation, thickens cervical mucous, thins endometrium
POP - time to effect
48 hours to take effect
When can the POP be started after delivery?
immediately after
POP - advantages
- Can be used when COCP is contraindicated.
- Periods may be less painful
- Not affected by broad spectrum Abx
POP - contraindications/cautions
Current breast cancer
considered safest method of contraception
POP - side effects
- Irregular menstrual bleeding
- Breast tenderness
- Acne
- Mood changes, decreased libido
- Ovarian cysts
Contraception - barrier methods
Mechanism of action = prevent sperm from entering the cervix.
Only method provide STI protection.
High failure rate (12-18%)
What are the options for emergency contraception?
- Emergency IUD
- Emergency Pill with Ulipristal Acetate (EllaOne)
- Emergency Pill with Levonorgestrel (Levonelle)
Emergency IUD
Insert before implantation occurs! (e.g. up to 5 days after unprotected sex or ovulation day)
99% efficacy
Can be used as contraception going forward (immediate protection)
Emergency Contraception - EllaOne
= 30 mg ulipristal acetate.
Within 5 days of UPSI (but it is better to take is ASAP)
95% efficacy
Progesterone receptor modulator
=> Interacts with progesterone (e.g. POP)
Cautions/CIs: • Previous ectopic • Severe malabsorption • Hepatic impairment • CYP450 inducing drugs • Progesterone (e.g. POP)
Emergency Contraception - Levonelle
= Levonorgestrel 1500 mcg (synthetic progesterone)
Can be used within 3 days of UPSI (but better to take it ASAP).
90% efficacy
Cautions/CIs: • Previous ectopic • Pregnancy • Severe malabsorption • Hepatic impairment
If BMI >26 / taking CYP450 inducing drugs Levonelle may not work - need double dose
Which emergency contraception may not work if BMI is too high?
Levonelle
Which emergency contraception may not work if the patient is taking the COC/POP for contraception normally?
EllaOne
Side effects of the morning after pills
- N&V
- Headaches
- Skin changes
- Menstrual cycle irregularities, next period earlier/later than expected
Safety netting for morning after pills
- If vomit within 3 hours, take another
- Take a pregnancy test in 3 weeks to ensure it worked
- Wait 7 days before restarting COC/POP
What are other factors to consider when providing Emergency Contraception?
Consensual intercourse/domestic violence
STI risk – assessment and screening
Ensure they are not already pregnant before offering EC
Starting long-term contraception as well
=> Cannot quick-start hormonal contraception with EllaOne as progesterone decreases it efficacy
What are some benign conditions of the vulva?
Bartholin’s Cyst Sebaceous Cyst Vulval Haematoma Lipoma/Fibroma/Myoma Condylomata Acuminata (genital warts) Simple Mesonephric (Gartner’s) or Paramesonephric Cysts Lichen Sclerosus Hypertrophic Vulval Dystrophy Vulval Intraepithelial Neoplasia
Bartholin’s Gland
Situated within the vestibule, just lateral to the introitus
Normally function to secrete a lubricating fluid.
Bartholin’s Cyst
Occurs when the duct of the gland becomes obstructed:
Palpable swelling (+/- pain)
Bartholin’s Abscess
occurs when a Bartholin’s cyst becomes infected
=> Extreme pain, lymphadenopathy, erythema
=> In rare cases causes systemic upset.
Management of Bartholin’s Abscess/Cyst
- Incision and drainage under local anaesthetic
- Abx for abscess
- Surgery may be required in recurrent cases.
Sebaceous Cyst of vulva
Infected sebaceous gland in the hair-bearing vulval skin.
Presents with a lump/swelling (+/- pain)
May require removal
What is Vulval Haematoma? How is it managed?
A result of direct violence/trauma – common in childbirth
Treated by incision and drainage
Simple Mesonephric (Gartner’s) or Paramesonephric Cysts
Represent embryologic remnants of the caudal end of the mesonephric (Wolffian) duct
What is Lichen Sclerosis ?
How is it managed?
= an inflammatory skin condition which typically affects the genital and anal areas of the body.
more common in women (particularly post-menopausal)
Can lead to malignant changes (5% develop squamous cell carcinoma)
Treatment – symptom control with emollients and topical steroid
Clinical features of lichen sclerosis
- Leucoplakia (thin, shiny and white skin) and inflamed/red
- Shrinkage and loss of labia minora
- Itching and/or pain (potentially after urination/sexual intercourse)
- Adhesions – can fuse labia together
Hypertrophic Vulval Dystrophy
= Squamous cell hyperplasia
Causes raised, thickened lesions (white/grey or red, depending on inflammation)
Histologically appears as dystrophy with no atypia
Treatment = topical steroids
Vulval Intraepithelial Neoplasia - presentation and risk factors
a pre-cancerous condition
Often asymptomatic, but there can be pruritis, pain, palpable lesions
RFs - HPV, HSV-2, smoking, immunosuppression, chronic vulvar irritation, lichen sclerosis
What accounts for the majority of vulval malignancies?
Squamous cell carcinoma (90%)
2nd most common = melanoma
What is the single most prognostic marker for vulval cancers?
lymph node status
also depends on lesion size and histological grade
Risk factors for vulval malignancy
HPV, VIN, CIN, Lichen sclerosus, Squamous hyperplasia, Immunodeficiency/immunosuppression, Hx genital warts, Hx cervical/vaginal cancer Smoking, alcohol
Vulval malignancy - clinical presentation
- Lump +/- lymphadenopathy
- Itching
- Vulval pain
- Pain/dysuria
Vulval malignancy - diagnosis
ANY vulval lesion warrants biopsy
Vulval malignancy - Treatment
- Wide local excision (stage Ia)
- Radical local excision plus ipsilateral groin node dissection (stage Ib and II)
- Radical vulvectomy
- Surgery + radiotherapy and chemotherapy
Bartholin Gland Carcinoma - diagnosis
rare;
often mistaken for benign cysts or abscesses
Honan’s criteria:
- The tumour is in the correct anatomical position
- The tumour is located deep in the labium majus
- Overlying skin is intact
- Some recognisable normal gland present
Bartholin Gland Carcinoma - Mx
Radical vulvectomy with bilateral groin and pelvic LN dissection
If it involves adjacent structures, post-op radiation and chemotherapy.
What are some benign cervical conditions?
- Cervical ectopy/ectropion
- Acute/chronic cervicitis
- Cervical polyps
- Nabothian Follicles
Cervical Ectopy
= when the columnar epithelium of the endocervix is visible as a red area around the os on the surface of the cervix
- Due to eversion
- A normal finding in young women.
- Can cause vaginal discharge/PCB
Cervical Ectropion
= a more irregular redness, resulting in minor lacerations during childbirth.
- Can cause vaginal discharge/PCB
- Can be treated by cryotherapy, without anaesthetic.
Cervical Polyps
= Benign tumours of endocervical epithelium.
Most common in women >40
May be asymptomatic or may cause IMB/PCB
Small polyps are avulsed without anaesthetic
what is Acute Cervicitis?
= acute ulceration and infection of cervix
Rare; often results from STD
occasionally found in severe degrees of prolapse when the cervix protrudes or is held back with a pessary.
What is chronic cervicitis?
How can it be managed?
= chronic inflammation and infection, often of an ectopy/ectropion.
Common cause of vaginal discharge
May cause “inflammatory smears”
Cryotherapy +/- Abx (depending on culture)
Nabothian Follicles
Squamous metaplasia can lead to obstruction of cervical glands and retention cysts form (Nabothian follicles/cysts).
Linked to chronic cervicitis
Why is cervical cancer considered preventable?
Long pre-invasive state
Cervical cytology screening programme
Treatment of pre-invasive lesions is effective
Risk factors for cervical cancer
age group 30-34 years = highest incidence
- Early sexual debut and increased number of sexual partners
- Parity
- Smoking
- Immunosuppression/deficiency
Protective factors against cervical cancer
HPV vaccination before sexual activity
Barrier contraception
HPV
HPV = circular, double-stranded DNA virus
80% of people will get HPV in their lifetime
More than 200 serotypes of HPV in total
Strongly associated with cervical cancer (Oncogenic HPV DNA is detected in >99% of cervical cancers)
How does HPV cause cervical cancer?
Infection of the cell with HPV results in the loss of important cell control mechanisms and the cell is more susceptible to malignant changes.
Cervical Intraepithelial Neoplasia
Grade depends on amount of dyskaryosis (abnormal nuclei).
- CIN I – atypical cells in 1/3 epithelium
- CIN II – atypical cells in 2/3 epithelium
- CIN III – atypical cells throughout
There is gradual progression from low-grade to high-grade without treatment.
Epithelium of the cervix
- The upper cervix (endocervix) is lined by a simple columnar epithelium that contains mucous-secreting cells.
- In contrast, the lower cervix (ectocervix) is lined by a stratified squamous epithelium.
- The transition zone between these two epithelia (the external os) is an area of metaplasia where the columnar epithelium has been replaced by squamous.
NHS cervical screening programme
Aim is to detect presence of HPV in the cervix
Starts at 25 years, then (if normal) every 3 years until age 49, then every 5 years until 64.
If HPV is found, the sample is then checked for abnormal cytology
=> If liquid cytology is normal, repeat screening in 12 months.
=> If liquid cytology is abnormal, then colposcopy is done to get a biopsy for histology.
Management of CIN
CIN I – Punch biopsy and repeat screening in 12 months
CIN II/III – Large Loop Excision of the Transformation Zone (LLETZ)
What happens in a LLETZ procedure?
What are the complications/risks?
= Excision of abnormal cells under LA (with diathermy to stop bleeding vessels)
Complications/risks:
- Post-op haemorrhage
- Cervical stenosis
- Small increased risk of preterm labour and PROM
Counselling post-LLETZ
Avoid tampons/intercourse/baths/swimming for 4 weeks.
One LLETZ treatment does not reduce fertility
May have some bleeding/brown discharge.
Cervical Glandular Abnormalities
Difficult to distinguish from severe dyskaryosis
High incidence of malignancy and high-grade lesions
=> Warrants early referral for biopsy
Types of Cervical Malignancy
- Squamous cell carcinoma (90%)
- Adenocarcinoma (10%)
- Other rarer types (melanoma, sarcoma, metastatic cancer, neuroendocrine cancer)
Cervical Malignancy - presentation
Abnormal vaginal bleeding – PCB/PMB/IMB
Vaginal discharge
Pelvic pain
OE - abnormal appearance and feel of the cervix
Staging of Cervical Cancer
I – Confined to cervix
II – Beyond cervix (but not lateral pelvic wall or lower 1/3 of vagina)
III – Pelvic wall / lower 1/3 of vagina
IV – Beyond true pelvis/bladder/rectum/distal mets
Cervical cancer - diagnosis and management
Diagnosis = via cervical biopsy.
Radiological staging = MRI, CXR, CT scan
IA – cone biopsy (preserves fertility)
IB/IIA – radical hysterectomy / trachelectomy
IIB + (or +ve lymph nodes) – radical hysterectomy, pelvic lymphadenectomy, chemoradiotherapy
Gynae cancers - palliative care
- Pain control
- N&V – antiemetics
- Heavy vaginal bleeding – high dose progesterones/radiotherapy
- Ascites/bowel obstruction – paracentesis, antiemetics, laxatives, antispasmodics
Benign conditions of the uterus
Fibroids Adenomyosis Polyps Endometriosis Haematometra Endometrial Hyperplasia
what is Haematometra?
= menstrual blood accumulating in the uterus because of outflow obstruction.
what is Endometrial Hyperplasia?
what is the main cause?
= Overflow of the glandular epithelium of the endometrial lining.
Usually occurs when a patient is exposed to UNOPPOSED OESTROGEN
Benign, but likelihood of malignancy increases in complex hyperplasia with atypia.
What are fibroids?
Who is more at risk?
Benign tumours of the uterine cavity (myometrial origin)
Vary in size and location (intramural, subserosal or submucosal)
More common in peri-menopausal women, afro-caribbean women, people with FHx of fibroids
What is the difference between uterine fibroids and polyps?
Fibroids = myometrial origin
Polyps = endometrial origin
Growth of fibroids
Growth is oestrogen and probably progesterone dependent
- Increases in pregnancy and with combined contraceptives.
- Slow/calcify after menopause (but HRT may maintain growth)
Fibroids - clinical presentation
~50% are asymptomatic and discovered only on pelvic/abdo examination or scan.
Sx: HMB (30%), IMB, dysmenorrhoea, urinary frequency/urinary retention, subfertility
Fibroids - investigation
- History and examination – palpable, solid mass in pelvis/abdo
- TV USS – shows mass continuous with uterus
- MRI/laparoscopy – distinguish from ovarian mass and adenomyosis
- Hysteroscopy – assess uterine distortion
- Bloods – Hb may be low if HMB, or high if fibroid secretes EPO.
Fibroids - management
If Asymptomatic – no treatment needed
Medical: preserves fertility
• GnRH and add-back HRT – temporary shrinkage
• Often used for 2-3 months pre-surgery
Surgical
• Myomectomy (if want to preserve fertility).
• Hysterectomy = most effective, but loss of fertility.
• Uterine artery embolization
Complications of fibroids
Torsion
Degenerations:
• RED – painful, haemorrhage, necrosis
• HYALINE/CYSTIC – liquified and soft
• CALCIFICATION – post-menopausal
Small risk of malignancy – leiomyosarcoma (0.1%)
What is adenomyosis?
= presence of endometrium with its underlying stroma within the myometrium.
Adenomyosis - clinical presentation
- Sx may be absent
- Painful, regular HMB is common
- OE – uterus is mildly enlarged and tender
Adenomyosis - management
IUS/COCP +/- NSAIDs to manage HMB/dysmenorrhoea
Often an indication for hysterectomy
What are uterine polyps?
Who is more at risk?
= small, benign tumours of the uterine cavity (endometrial origin)
RFs - women age 40-50 years, high oestrogen (e.g. tamoxifen)
Uterine polyps - clinical presentation and investigations
HMB, IMB
May prolapse through cervix
TV USS
Hysteroscopy
Uterine polyps - management
Hysteroscopic resection with diathermy
Avulsion (twist and tear off polyp with forceps)
what is Endometriosis?
Where does it occur?
What does it result in?
= endometrial tissue growth outside of the uterus.
Can occur anywhere in the pelvis
=> Most common = uterosacral ligaments & on/behind ovaries
Results in inflammation, progressive fibrosis, and adhesions.
Where is the most common location for endometriosis tissue?
uterosacral ligaments & on/behind ovaries
Risk factors for endometriosis
Oestrogen dependent – regresses after menopause
Risk factors:
- 30-45 years
- Nulliparous
- Genetics
Endometriosis - symptoms
- May be asymptomatic if mild
- Chronic pelvic pain (often cyclical, or can be constant)
- Dysmenorrhoea before menstruation (peaks day 1)
- Deep dyspareunia
- Pain on passing stools (dyschezia)
- Subfertility – ovarian problems, adhesions, tubal problems, peritoneal factors, endometrial factors.
Endometriosis - signs
- Retro-uterine/adnexal tenderness and/or thickening
- Uterus may be retroverted and immobile
- Nodule of endometrial tissue may be palpable on VE
Endometriosis - complications
Chocolate cyst (endometrioma) – accumulated, dark brown blood in ovaries
Frozen pelvis – pelvic organs immobile due to adhesions (very severe cases)
Chocolate cyst
= endometrioma
accumulated, dark brown blood in ovaries
occurs in endometriosis
Endometriosis - investigations
- History and physical examination
- Laparoscopy +/- biopsy gives definitive diagnosis
- MRI – to r/o adenomyosis
- Barium studies – to assess ureteric, bladder, bowel involvement.
Endometriosis - management
No treatment if asymptomatic
Medical (no improvement in fertility):
- Analgesia
- Back-to-back COCP/POP/GnRH/IUS
Surgical (may improve fertility):
- Laparoscopic ablation of lesions
- Adhesiolysis
- Drainage/removal of chocolate cysts
- TAHBSO
How common is Endometrial Cancer?
What is the most common type?
= 4th commonest female cancer (after breast, lung and bowel).
incidence is increasing
uncommon before age 40
Adenocarcinoma (columnar endometrial glands) account for 90%.
What % of PMB patients will have endometrial cancer?
~10%
but 90% of endometrial cancer cases present with PMB
Risk factors for endometrial cancer
Main cause = exposure to UNOPPOSED oestrogens.
Risk Factors:
- Early menarche (< age 12)
- Late menopause (> age 52)
- Infertility or nulliparity
- Obesity / Diabetes
- Treatment with tamoxifen for breast cancer
- Oestrogen replacement therapy after menopause
- Age >40
- Caucasian women
- FHx endometrial cancer or HNPCC
- PMHx of breast/ovarian cancer
- Prior radiation therapy for pelvic cancer
What factors reduce the risk of getting endometrial cancer?
- COCP – 50% reduction rate (but actual reduction is small because uncommon in women of child-bearing age).
- Tobacco smoking (smokers have lower levels of oestrogen and lower rate of obesity)
- Avoid weight gain
Endometrial cancer - presentation
Non-menstrual bleeding/discharge (especially PMB)
Endometrial cancer - Diagnosis and Staging
TV USS
Pelvic examination
Endometrial biopsy
Hysteroscopy – staging
MRI/CXR – assess spread
Endometrial cancer - stages
Pre-malignant = atypical hyperplasia.
I. Confined to uterine body
II. Involves cervix
III. Involvement of serosa, tubes/ovaries, vagina, parametrium, pelvic and paraaortic nodes.
IV. Bladder/bowel mucosa, distant mets
Endometrial cancer - management
Stage 1 – TAH BSO (+ post-op radiotherapy if high risk LN involvement)
Stage >1 – debulking surgery/radiotherapy.
Endometrial cancer - prognosis
Poor prognosis in advanced disease.
High recurrence rates
40% end up with chest mets
Ovary - anatomy
Outer cortex – germinal epithelium.
Inner medulla – connective tissue and blood vessels.
Cortex – follicles:
- Granulosa cells – secrete oestrogen
- Theca cells – also secrete oestrogen
Benign ovarian tumours
- 2 types – physiological and pathological
- May arise from any ovarian tissue.
- Most are cystic (fluid-filled), a few are solid.
What are physiological ovarian cysts?
Follicular Cyst
Luteal Cyst
physiological ovarian cysts - follicular
- Lined by oestrogen producing granulosa cells
- Can secrete oestrogen – cause menstrual disturbances and endometrial hyperplasia
physiological ovarian cysts - luteal
- Formed when corpus luteum does not regress
- Occurs on days 20-26 of cycle
What type of pathological ovarian cysts are more common in older or younger women?
Coelomic epithelium = more common in older women
Germ cell = more common in younger women
dermoid cyst/cystic teratoma
Derived from pluripotent germ cells.
Contain hair/skin/teeth
Asymptomatic.
Malignant form = solid teratoma
Serous cystadenoma
= Most common ovarian cyst
Thin, serous fluid content Epithelial lining (cuboidal/columnar)
Mucinous cystadenoma
Contain mucin
Can become enormous (cause pressure Sx on bladder and bowel)
Can rupture
5% become malignant
Ovarian cyst - Brenner cell tumour
Secrete oestrogen
Presents with asymptomatic vaginal bleeding.
Meig’s syndrome
= ovarian Fibroma + pleural effusion + ascites
Presentation of Benign Ovarian Cysts
Asymptomatic
Abdo/pelvic mass
Pressure Sx
Pain (variable)
Cyst Accidents
- Ruptur
- Torsion
Ovarian cyst - investigation
- Abdominal and pelvic exam – adnexal mass
- USS
- Tumour markers – Ca-125, beta-hCG, LDH, AFP, inhibin
- CT scan
- MRI
Ovarian cyst - management
Spontaneous resolution = most common
- Conservative/monitoring by scan +/- analgesia
- Laparoscopy – if cysts persist/presents acutely
- Ovarian cystectomy/oophorectomy
- Laparotomy +/- salpingo-oophorectomy +/- TAHBSO
How common is ovarian cancer?
What is the most common type?
30% of ovarian masses after menopause will be malignant
90% are epithelial carcinomas
=> of which 75% serous and 25% mucinous
=> In women <30, germ cell tumours are the most common
Ovarian cancer - risk factors
- Increased ovulation
- Low parity/nulliparous
- Early menarche
- Late menopause
- FHx BRCA1 and/or 2
- FHx HNPCC
what are some factors which protect against ovarian cancer?
Anything which decreases ovulation:
=> OCP, lactation, pregnancies
Ovarian cancer - signs and symptoms
• Most women are asymptomatic.
• Symptoms are often vague and non-specific – bloating, abdominal discomfort, pressure, nausea.
=> Similar to IBS Sx!!
- Mass, genital prolapse, ascites.
- Late – secondaries.
Ovarian cancer - diagnosis
A high index of suspicion.
USS abdo/pelvis
Ca-125
=> if under 40 years, assess AFP, beta-hCG and LDH in case germ cell tumour.
CT abdo/pelvis to assess spread
Ovarian cancer - staging
I. One/both ovaries only
II. Pelvic extension
III. Extra-pelvic extension
IV. Distant metastases
Ovarian cancer - management
Staging laparotomy and optimal debulking.
Aim to leave no macroscopic disease after surgery.
Stage 1c and above – LN dissection and post-op chemo.
If advanced/unfit for surgery – palliative care.
What is a pelvic organ prolapse?
What is the cause?
= protrusion of pelvic organs into vaginal canal
Caused by weakness of the surrounding structures
Types of pelvic organ prolapse
- Apical – uterus, cervix and upper vagina.
- Anterior vaginal wall:
- Cystocoele (bladder)
- Urethrocoele (urethra)
- Cysto-urethrocoele - Posterior vaginal wall:
- Rectocoele (rectum)
- Enterocoele (pouch of douglas)
Prolapse - risk factors
- Vaginal Delivery/pregnancy – large baby, long labour, instrumental
- Weakness of pelvic floor – inherited disease of collagen (e.g. Ehler’s Danlos), post-menopause, perineal damage, neuropathy/nerve damage
- Chronic increased intra-abdominal pressure – obesity, chronic cough/constipation, heaving lifting, pelvic mass
- Iatrogenic – pelvic surgery
Prolapse - presentation
- Lump/bulge/dragging sensation – worse at the end of the day/when standing
- Vaginal irritation/dryness/ulcers
- Need to push vagina back after straining
- Problems with sexual intercourse
- Bladder symptoms – frequency, urgency, voiding difficulties, recurrent cystitis.
- Bowel problems – obstruction of defecation, constipation, incomplete bowel emptying, faecal incontinence.
What factors may be important to ask in a Hx for someone with suspected prolapse?
- Any urinary/bowel symptoms?
- Sexually active?
Gynae Hx - Pre-/postmenopausal, contraception
Obstetric Hx
PMHx - chronic cough, obesity
DHx
Prolapse - investigations
Abdo examination – pelvic mass?
Pelvic examination – bimanual, speculum, vaginal mucosa
(Pelvic USS) – may be done to r/o pelvic mass or to investigate any PMB
Stages of uterine prolapse
Stage I – the uterus is in the upper half of the vagina.
Stage II – the uterus has descended nearly to the opening of the vagina.
Stage III – the uterus protrudes out of the vagina.
Stage IV – the uterus is completely out of the vagina.
Prolapse - management
CONSERVATIVE
- Lifestyle changes – weight loss, stop smoking
- Pessary (changed every 6-9 months)
- Pelvic floor exercises.
SURGICAL:
Fixation/ repair/ hysterectomy.
What does urinary continence rely on?
Bladder compliance
Efficient urethral sphincter
Efficient urethral support by pelvic floor and transmission of abdominal pressure.
Leakproof mucosal seal
What are the types of incontinence?
Which is the most common?
Stress incontinence (most common)
Overflow Incontinence
Urge Incontinence
What causes Stress Incontinence?
Caused by relaxed pelvic floor or increased abdominal pressure, often multifactorial:
- Pregnancy, obesity, age
- Vaginal delivery (long labour, forceps)
- Prolapse, hysterectomy
- Muscular diseases
Stress incontinence - presentation
Hx of leakage on exertion (e.g. cough/sneeze)
because increased IAP causes bladder pressure > urethral pressure
What causes overflow Incontinence?
Obstruction – pelvic surgery/strictures, BPH/prostate tumour, bladder calculi.
Detrusor failure – neurological, medication, DM.
Overflow incontinence - presentation
Hx of leakage on exertion or continuous flow/dribble
Occurs due to bladder distension
What causes urge incontinence?
Causes:
- Idiopathic
- Detrusor overactivity/overactive bladder – spinal cord injury/MS
- Previous pelvic surgery
Urge incontinence - presentation
Hx of urgency, frequency, nocturia (+/- stress incontinence).
Because detrusor contraction causes bladder pressure > urethral pressure.
What DHx might be particularly relevant in an incontinence history?
Diuretics, anticholinergics, anxiolytics/sedatives
Also: alcohol and caffeine intake
Examination of Incontinence
General – is the patient fit for surgery?
BMI
Abdominal exam – palpable mass/bladder?
Neurological exam
Pelvic exam:
- Bimanual – assess pelvic floor tone
- Speculum
- Vaginal mucosa – atrophy?
Incontinence - investigations
Urine dip - infection/DM?
Urinary diary
Post-micturition USS
CT urogram
Cystoscopy
Cystometry (bladder pressure studies)
How is cystometry performed?
Bladder pressure measured via catheter,
Abdominal pressure measured via rectum
Stress incontinence - management
Lifestyle – Weight loss, Pelvic floor exercises
Medical – duloxetine (SNRI for increased sphincter activity), injectable bulking agents
Surgical – colposuspension
Urge/overactive bladder incontinence - management
Lifestyle – decrease fluids and caffeince, medication review, bladder retraining
Medical – anticholinergics (to decrease detrusor activity), botulinum toxin A (to block neuromuscular transmission), intravaginal oestrogens.
What anticholinergics are used in incontinence?
What are side effects if these drugs?
e.g. oxybutynin, tolterodine, solifenacin
Side effects – dry mouth, constipation, blurred vision, cognitive dysfunction, CV effects
Overflow incontinence - management
Intermittent self-catheterisation
Treat underlying cause (e.g. BPH)
What is required for consent to be valid?
Patient must:
- Be competent to make a particular decision
- Have received sufficient information to make the decision
- Not be acting under duress, coercion or deceit.
What are the four parts to consent process?
- Understanding
- Retaining
- Deciding / weighing
- Communicating
Gillick Competence
minors of any age who are able to understand what is proposed and have sufficient discretion to be able to make a wise choice in their best interests, are competent to consent for medical treatment.
Fraser Guidelines
Apply specifically to sexual health and contraception
- The young person cannot be be persuaded to inform their parents or carers that they are seeking this advice or treatment (or to allow the practitioner to inform their parents or carers).
- The young person understands the advice being given.
- The young person’s physical or mental health or both are likely to suffer unless they receive the advice or treatment
- It is in the young person’s best interests to receive the advice, treatment or both without their parents’ or carers’ consent.
- The young person is very likely to continue having sex with or without contraceptive treatment.
What counts as domestic abuse?
= any incident / pattern of incidents of controlling, coercive or threatening behaviour, violence or abuse between those aged 16 or over who are or have been intimate partners or family members, regardless of gender or sexuality.
Disclosing cases of domestic abuse
The doctor cannot inform the police about cases of marital violence unless specific consent is obtained from the patient.
However, cases of DA can be shared without consent if it protects a child or public interest.
How does HIV infect cells?
What does this lead to?
HIV is a retrovirus, infecting lymphocytes with CD4 receptors.
The virus binds to the CD4 receptor and enters the cell.
It uses enzymes and the host DNA to make copies of itself and the CD4 cell gets destroyed in the process.
10 billion new HIV virions can be produced per day, with up to 2 billion CD4 cells killed each day. The decline in CD4 cells leads to immunosuppression.
Stages of HIV infection
- Acute HIV infection syndrome
=> patient is non-specifically virally unwell
=> viral load high; no anti-HIV antibodies - Stable, asymptomatic phase
=> viral load low; anti-HIV antibodies; stable CD4. - Symptomatic
=> signs of damaged immune system
=> Low CD4, any viral load
How long can the stable, asymptomatic phase of HIV last?
can last ~5-10 years for an average patient
HIV - monitoring disease
CD4 Count – a measure of immune function
• Predicts risk of opportunistic infection
• Normal range = 600-1200
• <200 = risk of opportunistic infection
Viral Load – a measure of viral replication
• Predicts rate of disease progression
• Aim for <50 copies/mL on treatment
At what CD4 count is opportunistic infection more likely?
CD4 <200
What is the aim for HIV viral load on treatment?
<50 copies/mL
HIV Transmission
Sexual transmission
=> Anal > vaginal > oral
IV drug use
Contaminated blood products
Vertical transmission
=> Mother to child
Why is testing for HIV important?
- Long asymptomatic stage of HIV infection – increased risk of transmission
- Treatment is very effective – near-normal life expectancy if treated early.
- Late diagnosis after the immune system is damaged leads to poorer prognosis
What is considered a late HIV diagnosis?
CD4 count <350 when diagnosed.
What is the most important predictor of morbidity and mortality in HIV?
CD4 count
HIV testing - consent
Consent is required before a HIV test.
Very few scenarios where it is appropriate to test for HIV without someone’s consent.
In what scenario is there universal offer for HIV testing
in specific clinical settings or with clinical indicator conditions.
=> Antenatal clinics, drug dependency programmes, TB services, blood-borne viruses, lymphoma, etc.
In what scenario is there universal HIV testing in GP practices?
Universal testing of GP registrants/acute admissions in high prevalence areas (>2 per 1000 population).
Regardless of symptoms and actual/perceived risk factors.
In what scenario is there targeted HIV testing offered?
based on demographics - people with potential risk factors
=> Regardless of symptoms
In what medical conditions is an HIV test indicated?
Anyone with one of the AIDs defining indicator conditions
HIV - 4th Generation test
Combined antibody and P24 antigen (part of the virus).
=> Window period of 6.5 weeks (45 days) – where someone has HIV but the test cannot detect it.
All positive tests confirmed with 2nd sample!
HIV - Point-of-care tests (POCTs)
4th generation POCTs
Drop of blood on test, wait 15 minutes.
=> Control result +/- positive HIV result.
All positive tests confirmed with 2nd sample!
HIV test result discussion
For most people – text message suggesting result is negative
=> Consider “window period” and re-test
=> Discuss ways of reducing risk
Face-to-face discussion if positive result or if negative but vulnerable/high risk/ difficulties understanding.
When is HIV treatment offered?
Anti-retroviral treatment is recommended for anyone with HIV
When CD4 count <200, prophylaxis against PCP (usually co-trimoxazole) is recommended.
90-90-90 UNAIDS target
90% with HIV are aware of HIV status.
90% of these people are on treatment
90% of those on treatment have an undetectable viral load.
what does Undetectable = untransmissible mean?
a person living with HIV who has an undetectable viral load does not transmit the virus to their partners.
Principles of HIV anti-retroviral therapy
A combination therapy to control the virus and minimise the chance of resistance.
=> Use of 2 or 3 drugs
Choose drugs that target at least 2 different stages of virus life cycle
Aim to maximise compliance - as few tablets as possible!
HIV therapy and drug interactions
Many of the antiretrovirals have quite significant drug interactions
HIV therapy side effects
- GI upset – nausea, diarrhoea
- Rashes and allergies
- Renal toxicity
- Liver toxicity
- Reduced bone mineral density
- Lipodystrophy and weight gain
- Increased cardiovascular risk/ blood pressure/ lipids/ blood sugars
- Peripheral neuropathy
HIV contact tracing
Aim = to break the chain of transmission by identifying those who may be at risk of an infection
For HIV, ideally all partners since the last negative test should be contacted.
HIV Prevention
Sexual Transmission
- Condoms
- PEP and PrEP
- Treatment as prevention (TasP) – undetectable = untransmissible
IVDU
- Needle exchanges
Vertical Transmission
- Appropriate ante- and post-natal care.
- If viral load is undetectable then vaginal delivery is possible!
- PEP for baby
Blood products
- Screening for HIV in blood products
Access to the genitourinary medicine service
GUM = branch of medical science concerned with diseases of the genital and urinary tract.
- Open access – no referral required.
- Strictly confidential – discrete building, separate patient records, etc.
Aims of GUM service
- Immediate diagnosis
- Effective, free treatment
- Partner notification
- Information/Sexual health education
Who is at risk of STIs?
Everyone!
Rates are higher in younger population (<25 years) and in MSM
Management of ?STI
History
Establish the diagnosis
- Examination
- Investigations
Treatment
- On the day where possible, stat doses
Counselling, education, health promotion
Partner notification
?STI - History
Symptoms
PMHx
- Including past STIs
DHx, allergies
Women – menstrual cycle, obstetric Hx, contraception, cervical cytology, HPV vaccine.
SHx – recreational drugs, alcohol, smoking, domestic violence, chemsex
Sexual Hx
BBV risk assessment
What is chemsex?
Use of drugs in a sexualised context, leading to more sexually disinhibited behaviour
STI Sx - Male
Discharge Dysuria Urinary frequency/haematuria Testicular pain/swelling Rashes/ulcers/lumps Rectal symptoms in MSM -- Asymptomatic screening STI contact
STI Sx - Female
Unusual discharge Dysuria/Urinary frequency/haematuria Itching/soreness Pelvic/lower abdominal pain Dyspareunia (superficial/deep) Rashes/ulcers/lumps IMB and PCB -- Asymptomatic screening STI contact
What is the most prevalent bacterial STI in the UK?
chlamydia
Chlamydia trachomatis
Intracellular gram-negative bacteria
Infects columnar and transitional epithelium
Can infect the cervix, urethra, rectum, conjunctivae and pharynx.
Sexual transmission (vaginal, anal, oral sex) is most common route of infection, but vertical transmission is also possible.
RFs for chlamydia infection
- Condomless sex
- New partner within the last year
- Age <25
Chlamydia - presentation
Often asymptomatic (especially pharyngeal and rectal infections)
Women: • Increased discharge (watery/milky) • AUB • Cervicitis • Dysuria
Men:
• Dysuria
• Urethral discharge
Chlamydia - complications
PID (chronic pelvic pain, subfertility)
Increased risk of ectopic pregnancy,
Reiter’s Syndrome,
Neonatal conjunctivitis.
Reiter’s Syndrome
= urethritis, conjunctivitis, arthritis.
Chlamydia - diagnosis
Men – first catch urine (FCU) for NAAT analysis.
Women – endocervical/vaginal swab for microscopy.
Chlamydia - management
- Doxycycline PO 7 days o.d.
- OR azithromycin PO stat dose.
Neisseria gonorrhoea
gram-negative intracellular diplococcus
Infects the mucous membranes of the urethra, endocervix, rectum, pharynx and conjunctiva.
Transmission occurs by direct transmission from one infected mucous membrane to another – primarily through sexual contact, but vertical transmission also occurs.
Gonorrhoea - presentation
Often asymptomatic
White/yellow discharge (M&F)
Urethritis
Bartholinitis
Cervicitis
Super-gonorrhoea
multi-drug resistant gonorrhoea
Gonorrhoea - complications
bacteraemia,
acute septic arthritis,
PID,
neonatal conjunctivitis.
Gonorrhoea - diagnosis
Men – FCU for NAAT analysis
Women – endocervical swab for microscopy (looking for gram -ve diplococcus).
!!Culture to check ABX sensitivities!!
Gonorrhoea - management
Treatment = IM ceftriaxone.
Alternative = ciprofloxacin, but resistance is common.
trichomonas vaginalis
a flagellated protozoan
Can be found in the vagina, paraurethral glands, sub-preputial sac and penile lesions.
Main transmission is through vaginal intercourse.
Trichomoniasis - RFs
> 90% of diagnoses in women
=> Rates are highest in women of black ethnicity.
Trichomoniasis - Presentation
May be asymptomatic
Vaginal discharge
- Vary in colour and texture
- Grey/green/yellow
- Offensive smell
Vulval itching or pain
Dysuria (M&F)
Trichomoniasis - Complications
preterm/LBW child,
post-partum sepsis,
HIV transmission.
Trichomoniasis - Diagnosis
High vaginal swab
Wet film microscopy
Trichomoniasis - Management
Treatment = metronidazole PO stat dose.
treponema pallidum
a spirochete bacterium, causing syphilis infection
Transmitted by sexual contact, vertical transmission from mother to child or transmission by infected blood products.
Early syphilis
= when the person has been infected within the last 2 years.
It can be asymptomatic (early latent) or symptomatic (primary or secondary).
Late syphilis
= when the person has been infected for >2 years.
It can be asymptomatic (late latent) or symptomatic (tertiary).
Syphilis - RFs
MSM
Syphilis - Presentation
Primary syphilis – chancre (painless genital/mouth ulcer).
Secondary syphilis:
- Fever, myalgia, headache, lethargy, malaise, anorexia.
- Rash (soles/palms)
- Warty genital and peri-oral growths (condylomata lata)
- Multi-organ problems
Tertiary Syphilis:
- CV system – aortic regurgitation
- Skin/bony swellings (gummata)
- Neurological – Dementia, Tabes dorsalis
Syphilis - diagnosis
Serological tests.
Syphilis - management
Treatment – IM/IV penicillin.
10-14 days PO doxycycline if penicillin allergic.
What causes genital warts?
HPV type 6 and 11 cause most genital warts (responsible for >75% of warts but are low-risk strains).
Transmitted by skin-to-skin contact (usually sexual)
Do condoms reduce the risk of transmission of genital warts?
condoms reduce the risk of transmission by ~30-60%.
Genital warts - presentation
Multiple warts
- Varied appearance,
- External or internal
- Flesh-coloured or pigmented
Genital warts - diagnosis
Diagnosed on inspection.
Genital warts - management
Topical podophyllin/imiquimod cream
Cryotherapy
Prevention – HPV vaccination
What causes genital herpes?
Caused by HSV 1 and 2
Transmitted by skin-to-skin contact (vaginal/anal/oral sex or genital-to-genital contact).
Can be transmitted when individuals have no symptoms (asymptomatic shedding).
Genital herpes - presentation
Can be asymptomatic (1/3 develop symptoms).
Multiple, small, painful vesicles.
Dysuria and itchy genitals
Malaise, fever, headache
Local lymphadenopathy.
Genital herpes - complications
secondary bacterial infection,
acute urinary retention,
neonatal herpes (high mortality).
Can lie dormant in dorsal root and reactivate at a later time
Genital herpes - diagnosis
Diagnosed by inspection and PCR of viral swabs.
Genital herpes - management
Treated with acyclovir.
What is Bacterial Vaginosis?
this is NOT an STI.
Caused by a disturbance in the normal vaginal bacteria – makes the vagina slightly less acidic than normal and this encourages the growth of anaerobic bacteria and fewer normal lactobacilli.
BV - presentation
grey/white discharge with fishy odour
BV - complications
preterm labour
BV - diagnosis
high vaginal swab,
raised pH,
“clue cells” on microscopy
BV - management
Metonidazole 400 mg twice a day for 5-7 days.
OR topical metronidazole gel for 7 days
Or topical/PO clindamycin
What is candidiasis/thrush?
This is NOT an STI.
Caused by candida albicans
Candidiasis - RFs
immunocompromise,
diabetes,
pregnancy,
ABX use
Candidiasis - presentation
often asymptomatic, “cottage-cheese” discharge, vulval itching, dyspareunia, dysuria.
Candidiasis - diagnosis
high vaginal swab for culture
Candidiasis - management
antifungal pessary/cream (clotrimazole)
or oral fluconazole (NOT if pregnant).
What is the window period for STI testing?
= the time from infection to the time detectable by testing.
Gonorrhoea and chlamydia – 2 weeks
Blood-borne viruses – 6 weeks.
Menstrual Hx
Duration of bleeding and length of cycle
Frequency/regularity of periods
Volume of bleeding:
- Heavier than normal?
- Soaking through pads?
- Impacting day to day life?
Menarche
Contraception
Gynae Hx
Previous gynae problems?
Previous gynae surgery?
Cervical screening:
- Confirm date of last smear test
- Confirm HPV vaccination status
Contraception
Menstrual Hx
Obstetric Hx
Gravidity and Parity
Outcome of pregnancies
Gather key details about the patient’s current pregnancy (if relevant)
- Gestation
- Sx associated with pregnancy (e.g. N&V, back pain)
- Complications
- Recent scan results
Sexual History
Last sexual contact:
- Timing – when?
- Consensual?
- Regular sexual partner or casual?
- Clarify the sex and country of origin of the partner
- Clarify the type of sex involved (Vaginal/anal/oral)
- Contraception (Barrier and other forms)
Ask about other sexual partners in the last 3 months.
BBV risk assessment
“Have you ever had a partner who is known to be HIV positive?”
“Have you ever had sex with a bisexual man/engaged in male homosexual activity?”
“Have you ever had sex with someone abroad, or who was born in a different country?”
“Have you ever injected drugs?”
“Are you aware of any of your previous partners having ever injected drugs?”
“Have you ever paid someone for sex, or been paid for sex?”
What extra components are there in an O&G history?
- Menstrual History
- Obstetric History
- Contraception
- Date of last cervical smear
+/- Sexual History
Gravidity
= number of times a woman is/had been pregnant (regardless of pregnancy outcome).
Parity
= number of pregnancies reaching a viable gestational age [24 weeks] (including live and stillbirths)
When should you start asking about foetal movements?
After 20 weeks
What is the definition of chronic pelvic pain?
= intermittent or constant pain in lower abdomen or pelvis of at least 6 months duration, not occurring exclusively with menstruation or intercourse and not associated with pregnancy.
Chronic pelvic pain - Cyclical pain
Related to reproductive system (endometriosis/ adenomyosis)
Respond to ovarian suppression
Chronic pelvic pain - Non-cyclical pain
- Adhesions
- PID
- Malignancy
- GI/urological/neurological/MSK
Chronic Pelvic Pain - Diagnosis
History
Examination
- BMI
- Abdominal exam
- Vaginal exam
- Triple swabs for infection screening
Investigations
- Transvaginal USS
- MRI
- Laparoscopy = GOLD-STANDARD but 2nd line
Chronic Pelvic Pain - Management
Therapeutic options depend on diagnosis:
- Appropriate analgesia
- IBS – trial of antispasmodics/diet
- Cyclical pain – Trial with COCP/ GnRH analogue for 3-6 months
- Psychological – counselling and psychotherapy
- Referral to pain management team/pelvic pain clinic/other specialities
Pelvic Inflammatory Disease
= infection of the cervix, uterus, tubes and contiguous structures.
Causes of PID
Usually caused by ascending bacteria from sexually transmitted infection.
Uterine instrumentation or retained products of conception are non-sexually transmitted causes.
PID - Presentation
Often asymptomatic until complications present.
- BILATERAL lower abdo pain
- Abnormal PV bleeding/discharge
- N&V
- Deep Dyspareunia
• RUQ pain (Fitz Hugh Curtis Syndrome – perihepatic irritation).
PID - Diagnosis
OE:
• Pyrexia, Tachycardia
• Abdominal rigidity/peritonism
• Tender uterus and bilateral adnexae, cervical excitation
Ix:
• Pregnancy test – r/o ectopic
• WCC and CRP – raised
• Blood cultures if pyrexial
• Endocervical swabs – gonorrhoea and chlamydia
• Pelvic USS – r/o abscess/ovarian cyst
• Laparoscopy + fimbrial biopsy & culture = GOLD STANDARD
PID - Management
• Analgesia
• ABX
=> IM Ceftriaxone + PO doxycycline + PO metronidazole (empirical)
Review at 24 hours
If septic – admission and sepsis 6 and senior review
PID - Complications
Abscess/Pyosalpinx
Tubal obstruction/subfertility
Chronic pelvic infection/pain
6x increased risk of ectopic pregnancy
Important points for early pregnancy scanning
We do not expect to see anything meaningful on a scan until 6 weeks of pregnancy
Interpreting scan results in the context of the patient’s history, examination findings and blood results is vital.
Definition of miscarriage
when the foetus dies or delivers dead before 24 weeks.
Usually occurs before 12 weeks.
How common is miscarriage?
What is the most common cause?
Occurs in ~15% of pregnancies
Cause is significant chromosomal abnormality in ~60% of cases.
Miscarriage - Sx
- Lower abdominal pain (crampy, “period-like”)
- Vaginal bleeding (often before pain)
Miscarriage - Investigations
Speculum – open os suggestive of miscarriage.
TV USS – shows if foetus is intrauterine/viable or any retained products of conception.
48-hour serum hCG – rise >66% in viable pregnancies, low in miscarriage.
Check FBC, Rhesus Status, G&S
CRP – often raised in miscarriage
crown-rump Length (CRL) <7.2mm on 1st scan
this could either be a very early pregnancy OR a miscarriage.
=> Re-scan in 7-10 days.
CRL >7.2mm and no cardiac activity on 1st scan
miscarriage is diagnosed (at this size a heartbeat should be present).
Threatened miscarriage
Os Closed,
Uterus normal for date
Foetus still alive (only 25% miscarry)
Inevitable miscarriage
Os Open
Pain, heavy bleeding
Foetus may/may not be alive
Incomplete miscarriage
Os open
USS – some RPOC
Pain, bleeding
Some foetal parts passed
Complete miscarriage
Os closed
USS – no RPOC
Slowed bleeding
ALL foetal parts passed
Missed Miscarriage
Os closed
Uterus small for date
May be asymptomatic
Often found on routine scan where no FHR is detected
Septic miscarriage
Uterine tenderness
Endometritis
Pain
Offensive vaginal loss
+/- fever
management of miscarriage
Anti-D prophylaxis needs to be given if Rh -ve and pregnancy >12 weeks’ gestation, as miscarriage is a sensitising event.
- Conservative/Expectant – wait to see if the miscarriage occurs naturally (~80% success)
- Medical:
- Surgical
Inevitable, incomplete, and missed miscarriages can be managed with all 3 options.
Septic miscarriage is managed with antibiotics and surgical management
Miscarriage - conservative management
Review after 14 days.
No bleeding/pain – pregnancy test at 3 weeks to confirm miscarriage.
Still bleeding/pain – consider medical/surgical management.
Miscarriage - medical management
PO/PV misoprostol and mifepristone
Also analgesia and anti-emetics PRN
Pregnancy test at 3 weeks to confirm miscarriage
Risks – bleeding, infection, failure
Miscarriage - surgical management
Vacuum aspiration and histological examination to exclude molar pregnancy
Complications - infection, partial removal of endometrium, perforation/scarring of uterus (causing Asherman’s Syndrome)
What is considered recurrent Miscarriage?
3 or more miscarriages in succession – affects ~1% of couples.
Causes of recurrent miscarriage
- Antiphospholipid antibodies
- Chromosomal defects
- Uterine abnormalities – e.g. LLETZ, fibroids
- Hormonal – e.g. thyroid problems, uncontrolled diabetes.
- Other – obesity, smoking, PCOS, higher maternal age
Ectopic pregnancy
= a pregnancy that is growing anywhere outside the uterus.
Most common location is the fallopian tubes/ampulla.
ectopic pregnancy - Risk factors
= anything that can scar the tubes:
- Advanced maternal age
- Previous ectopic pregnancy
- IVF pregnancy
- PMHx chlamydia/pelvic infection/PID
- Previous abdo/tubal surgery
- Use of POP or IUD
Ectopic pregnancy - presentation
Can be variable/vague/asymptomatic
Lower abdominal pain
Rebound tenderness
Uterine and adnexal tenderness
Abnormal vaginal bleeding
Signs of intraperitoneal blood loss
Amenorrhoea 4-10 weeks
Uterus small for date and closed cervical os.
What can be signs of intraperitoneal blood loss
- Dizziness
- Shoulder-tip pain (referred)
- Syncope/collapse
Ectopic pregnancy - Investigations
In a woman of child-bearing age, abdominal pain and abnormal PV bleed = ectopic until proven otherwise
=> MUST do a urine pregnancy test!
- Urine hCG pregnancy test (+ve in ectopic)
- TV USS
- Serum beta-hCG to distinguish early and ectopic pregnancies
- Laparoscopy
=> Most sensitive, but invasive – rarely used.
How to differentiate early pregnancy and ectopic pregnancy with serum beta-hCG?
Early pregnancy – increase by >60% in 48 hours.
Ectopic – slower increase or decrease.
If already >1000 IU/mL, you would see the pregnancy in the uterus unless it was ectopic.
Ectopic pregnancy - management
- Admit to hospital – A-E assessment, IV access, X-match, Anti-D if Rh -ve.
- Medical = methotrexate (if small, un-ruptured)
- Surgical
- Counselling
What are the requirements of an ectopic pregnancy to be suitable for medical management?
How is medical management done?
if unruptured, no cardiac activity and hCG <3000 IU/mL
Single dose methotrexate (15% need 2nd dose, 10% need surgical escalation)
Followed by serial hCG level monitoring.
Surgical management of ectopic pregnancy
Laparoscopic salpingectomy (tube removal)
Consider salpingostomy (remove ectopic and leave tube) if other tube is damaged, for future conception.
Counselling for ectopic pregnancy
Explain the need for serial hCG levels to confirm removal of ectopic.
Make aware of warning signs of rupture – severe abdo pain, pale/clammy, tachycardic, LOC/collapse.
Information about increased risk of ectopic (but reassure that many go on to have successful pregnancy in the future).
Emotional support/counselling.
Definition of Hyperemesis Gravidarum
Severe N&V in pregnancy that leads to:
- Dehydration
- Electrolyte disturbances
- Weight loss
- Ketosis
Hyperemesis Gravidarum - presentation
Excessive vomiting
Symptoms suggestive of dehydration (e.g. oliguria and syncopal episodes)
Hyperemesis Gravidarum - risk factors
- Multiparous
- Multiple pregnancy
- Molar pregnancy
Hyperemesis Gravidarum - DDx
- UTI
- Gastroenteritis
- Trophoblastic Disease
Hyperemesis Gravidarum - Investigations
BP and Pulse – ?hypovolaemia
Urine dip:
=> Ketonuria suggests dehydration/starvation
=> (r/o UTI)
FBC, U&E, LFT
Calcium
=> r/o hypercalcaemia (can cause vomiting)
Pelvic USS
=> Check viability of pregnancy
=> Check for situations where hyperemesis is more likely.
Hyperemesis Gravidarum - Management
Dehydration:
=> IV fluids (Hartmann’s/saline)
N&V:
=> Antiemetics – promethazine, cyclizine, metoclopramide, ondansetron (IV/IM/SL if oral intake not tolerated)
Close monitoring – BP, pulse, renal function
What is Gestational Trophoblastic Disease?
Occurs when the trophoblastic tissue of the blastocyst proliferates more aggressively than normal.
- HYDATIDIFORM MOLE
- INVASIVE MOLE
- CHORIOCARCINOMA
Gestational Trophoblastic Disease - Hydatidiform Mole
localised and non-invasive proliferation.
Complete:
• Sperm fertilises the empty oocyte = mitosis of 46XX tissue
• No foetal tissue and no foetal RBCs
Partial:
• Two sperms fertilise the oocyte = forms triploid zygote 69XXX/XXY/XYY
• Viable evidence of foetus (but abnormal)
Gestational Trophoblastic Disease - Invasive Mole
invasion localised to within the uterus
Gestational Trophoblastic Disease - choriocarcinoma
invasion followed by metaplasia outside of the uterus
Gestational Trophoblastic Neoplasia
= malignant transformation of the trophoblastic tissue.
Diagnosed when persistently elevated hCG/persistent vaginal bleeding/blood-borne metastases resulting from persistence of any of the above.
Risk factors for Gestational Trophoblastic Disease
- Asian ethnicity
- Extremes of maternal age
- Previous molar pregnancy
- Familial/sporadic clusters of biparental complete hydatidiform mole.
Gestational Trophoblastic Disease - Presentation
- Vaginal bleeding in early pregnancy (non-specific sign)
- Severe vomiting/Hyperemesis
- Uterus large for date
- Early onset pre-eclampsia / hyperthyroidism
Gestational Trophoblastic Disease - Investigation
Serum hCG – very high
USS – characteristic “snowstorm” appearance
Histology = diagnostic
Gestational Trophoblastic Disease/Neoplasia - Management
Gold standard management = surgical evacuation of the uterus.
=> The resulting products of conception should be analysed in the laboratory to confirm the diagnosis.
=> Anti-D prophylaxis recommended
Serial hCG levels – if remain persistent or rising, this suggests malignancy.
Management of GTN:
=> Chemotherapy.
=> Only 3 specialist centres in the UK deal with these
Prevention of infection in pregnancy
- Seasonal vaccination against influenza (and Covid)
- Vaccination against rubella
- Avoidance of individuals with chickenpox
- Avoidance of foods that may harbour Listeria – e.g. soft cheeses
Routine Antenatal Screening - Syphilis, HepB, HIV
Pyrexia in pregnancy
Can be normal => pregnancy results in a progressive and significant increase in endogenous heat production.
Antipyretics in a febrile pregnant woman are important to help prevent intrauterine hyperthermia and possible foetal damage
Most common organisms causing maternal sepsis in pregnancy
Group A Strep and E. coli
Maternal Sepsis - Presentation
Symptoms can be non-specific – diagnosis is very challenging
- D&V,
- Fever (but may be absent or even low in some cases)
- Abdominal pain,
- Tachycardia, Tachypnoea
- Confusion
• Offensive vaginal discharge/Productive cough/ Urinary symptoms/ rash
Maternal Sepsis - management
- Urgent and repeated microbial specimens
=> BLOOD CULTURES
=> Consider sputum sample, throat swab, MSU, wound swab, etc. - Appropriate IV antibiotic therapy.
=> Parenteral broad-spectrum immediately (within 1 hour), without waiting for microbiology results. - Fluid balance - input/output
- Oxygen if needed
- Serum lactate should be measured
=> Also FBC, U&E, ABG - Relevant imaging to confirm source of infection.
Chorioamnionitis
= inflammation of the amniochorionic membranes of the placenta (typically in response to microbial infection).
Usually polymicrobial cause
what is the greatest risk factor for developing Chorioamnionitis?
preterm pre-labour rupture of membranes
Chorioamnionitis - diagnosis
- Maternal pyrexia
- Maternal tachycardia
- Uterine tenderness
- Offensive vaginal discharge
- Foetal tachycardia
Chorioamnionitis - management
Augment delivery if not already in established labour.
Broad spectrum IV antibiotics
Antipyretics and keep well-hydrated
Send FBC, blood cultures, low vaginal swab and MSU for analysis.
TORCH infections
toxoplasmosis, rubella, CMV, HSV
How is congenital syphilis prevented in a syphilis sero-positive pregnant mother?
pregnant woman treated with penicillin
Management of Chlamydia infection in pregnancy
Antibiotic Tx is necessary to prevent vertical transmission to the neonate
Azithromycin / Erythromycin / Amoxicillin
Test of cure (TOC) is recommended in pregnancy – 3 weeks following the completion of Abx treatment
Which chalmydia Tx should be avoided in pregnancy?
Doxycycline and ofloxacin are contraindicated in pregnancy
Implications of rubella infection on pregnancy
If rubella infection occurs in the first 16 weeks, implications are substantial.
=> cardiac defects, IUGR, eye defects, liver/bowel/spleen abnormalities
If 16-20 weeks, implications are deafness only
What cardiac defects can be caused by Congenital rubella syndrome?
Pulmonary artery stenosis
Patent ductus arteriosus
Maternal Parvovirus infection
Main effect = foetal anaemia
Infection in the first 20 weeks can lead to intrauterine death and hydrops fetalis
Congenital CMV
= most common congenital infection
Microcephaly, IUGR, hepatosplenomegaly, ascites, jaundice, seizures
What happens if maternal infection with varicella zoster occurs at term?
Elective delivery should normally be avoided until 5-7 days after the onset of maternal rash to allow the passive transfer of antibodies from mother to child
Effects of sodium valproate on foetus
Birth defects (10% of babies exposed) => Spina bifida, facial and skull malformations, limb/cardiac/renal and urogenital malformations
Developmental defects (30-40% of babies exposed)
Sodium valproate and pregnancy
Causes birth/developmental defects
Valproate MUST NOT be used in any woman/girl able to have children, unless she has a pregnancy prevention programme in place.
Indications for 5mg daily folic acid
5mg folic acid daily is required if the patient or partner:
- Had an NTD
- Had a previous baby with NTD
- Have FHx of NTD
- Have diabetes
Normal folic acid dose
Standard dose = 400mcg Folic Acid daily pre-pregnancy and for first trimester
Placental transfer of drugs
Nearly all drugs, except those with a very high molecular weight (e.g. insulin and heparin) cross the placenta to the foetus
Lipid-soluble un-ionised drugs cross the placenta more rapidly
Highly protein-bound drugs cross the placenta to a lesser extent
What factors affect the degree of harm to the foetus by maternal medications?
The effect of drug exposure depends on:
- Timing of exposure
- Dosage and duration
- Genetic susceptibility
- An element of chance
Timing of drug exposure - Pre-embryonic period
Until 14 days post-conception
“All or nothing”
=> Damage to all/most cells => death
=> Damage to only a few cells => normal development
Timing of drug exposure - Embryonic period
Week 3-8
Most important phase for teratogenicity
Major organ systems forming
Timing of drug exposure - Foetal period
(week 9 onwards):
Baby less susceptible to toxic insults
Although some organs (cerebellum and urogenital structures) are still developing.
Lower risk drugs in pregnancy
Antacids Paracetamol Penicillins, Cephalosporins Laxatives Inhaled asthma medications
(Generally considered okay to prescribe if needed)
High risk drugs in pregnancy
ACEi Phenytoin/Sodium Valproate Lithium Isotretinoin/retinoids Alcohol Misoprostol Warfarin
(AVOID!)
1st line anti-emetics in pregnancy
Cyclizine,
Promethazine
Foetal defects caused by lithium
Cardiovascular Defects (Ebstein’s anomaly of the triscuspid valve)
drugs that inhibit/reduce breastmilk production
Bromocriptine, diuretics, anabolic steroids
Regular moderate/heavy alcohol consumption
High risk drugs in breastfeeding
Ciclosporin Lithium Ecstasy / other illicit drugs Amiodarone Alcohol Tetracyclines Quinolones
How can gestational diabetes be diagnosed?
=> ‘5678’
Fasting glucose is >/= 5.6 mmol/L,
or
2-hour glucose level of >/= 7.8 mmol/L
Whirlpool Sign
Twisting of the structure on USS / CT
Indicates ovarian torsion
NICE guidelines - indications for measuring Ca-125
CA125 should be performed if a woman (especially if aged 50 years old or over) has any of the following symptoms on a regular basis:
Abdominal distension or ‘bloating’
Early satiety or loss of appetite
Pelvic or abdominal pain
Increased urinary urgency and/or frequency
Pregnancy and the MMR vaccine
MMR vaccines should not be administered to women known to be pregnant or attempting to become pregnant
Women should avoid becoming pregnant for 28 days after receipt of MMR vaccine
C-section categories
CAT 1
An immediate threat to the life of the mother or baby
Delivery of the baby should occur within 30 minutes of making the decision
CAT2
Maternal/foetal compromise which is not immediately life-threatening
Delivery of the baby should occur within 75 minutes of making the decision
CAT3
Delivery is required, but mother and baby are stable
CAT4
Elective C-section
Indications for Category 1 C-section
Examples indications include:
Suspected uterine rupture, Major placental abruption, Cord prolapse, Foetal hypoxia Persistent fetal bradycardia
