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
