Obstetrics Flashcards
Describe the features of an obstetric history
- Key details: gestational age, gravidity, parity
- Presenting complaint and history
- Focussed questioning of symptoms
- Current pregnancy: gestation, scan results, screening, immunisations, mental health, MoD
- Previous pregnancy: gestation at delivery, birth weight, MoD, complications, other pregnancies (miscarriage, termination, ectopic)
- Gynaecological history: cervical screening, previous conditions and treatments
- Past medical history
- Drug history and allergies
- Family history: inherited conditions, pre-eclampsia, diabetes
- Social history
What are the common symptoms in an obstetric history?
- Nausea and vomiting: common, hyperemesis gravidarum is a serve form with electrolyte disturbance, weight loss, and ketonuria
- Reduced foetal movements: associated with foetal distress
- Vaginal bleeding: cervical bleeding (e.g. ectropion), placenta praevia, placental abruption
- Abdominal pain: UTI, constipation, pelvic girdle pain, placental abruption
- Vaginal discharge or fluid loss: STIs, rupture of membranes
- Headache, visual disturbance, oedema, epigastric pain: pre-eclampsia
- Pruritis: obstetric cholestasis
- Unilateral leg swelling: DVT
- Chest pain and SOB: PE
- Systemic symptoms: fatigue (anaemia), fever (chorioamnionitis), weight loss (hyperemesis gravidarum)
What is gestational age?
- Used to describe ‘how far along’ a pregnancy is
- Counted from the first day of the last menstrual period (LMP), or 2 weeks before conception
- A normal pregnancy is between 38-40 weeks
What are the stages of labour
- First stage: from the onset of labour until the cervix is fully dilated (10cm)
- Second stage: from full cervical dilation until the baby is delivered
- Third stage: after the baby is delivered until the delivery of the placenta
Define gravidity and parity
- Gravidity: the number of times a women has been pregnant
- Parity: the number of times a women has given birth to a foetus older than 24 weeks (alive or stillbirth)
Define nulliparous, primiparous, and multiparous
- Nulliparous: never delivered a baby
- Primiparous: delivered one baby (often used interchangeably with primigravida but not technically correct)
- Multiparous: delivered more than one baby
Describe the first stage of labour
- Involves cervical dilation and effacement (thinning and shortening)
- Split into latent phases (0-3cm dilated, irregular contractions) and active phases (4-10cm, 3/4 strong contractions in 10 mins)
- Rate of dilation is between 1-3cm/hour, and the time to full dilation varies greatly (generally shorter with higher number of previous pregnancies)
Describe the second stage of labour
- Passive phase: from full dilation until the head reaches the pelvic floor and the woman experiences the urge to push
- Active phase: when mother is pushing with her contractions
- Success depends on… power (strength of uterine contractions), passenger (size, posture, lie, presentation of foetus), passage (size/shape of the pelvis)
How long is each stage of labour?
- First stage: nulliparous = 8-18 hours, multiparous = 5-12 hours
- Second stage: nulliparous = no more than 3 hours, multiparous = no more than 2 hours
- Third stage: often less than 10 minutes, no more than 30 minutes
Describe the cardinal movements of labour?
- Engagement: baby enters pelvic inlet
- Descent: baby moves lower into pelvic cavity
- Flexion: foetal skull flexes (most favourable presentation due to smallest diameter)
- Internal rotation: contact with levator ani tuns occiput anteriorly
- Extension: pubic symphysis acts as fulcrum so that foetal head extends and crowns
- Restitution/external rotation: head rotates so that shoulders are in AP direction
- Expulsion (delivery): external traction downwards the deliver anterior shoulder, then upwards to deliver posterior shoulder
What are Braxton-Hicks contractions?
- Occasional irregular contractions of the uterus
- Felt during the second and third trimester
- Do not indicate the onset of labour, known as ‘practice’ contractions
Describe the foetal lie, presentation, and position
- Lie: relationship between long axis of the foetus and the mother (longitudinal, transverse, oblique)
- Presentation: the foetal part that first enters the maternal pelvis (cephalic, breech, shoulder, face, brow)
- Position: orientation of the foetal head as it exits the birth canal (occipito-anterior = foetal occiput faces anteriorly/posteriorly/transverse)
Define pre-eclampsia
New onset of hypertension (over 140 systolic or 90 diastolic) and proteinuria after 20 weeks of pregnancy, and the coexistence of 1 or more of the following new-onset conditions:
- renal insufficiency
- liver involvement (high ALT/AST w/wo abdo pain)
- neurological complications (seizures, altered mental state, severe headache, clonus, stroke)
- haematological complications (low platelets, DIC, haemolysis)
- uteroplacental dysfunction (foetal growth restriction, abnormal umbilical artery, stillbirth)
Define eclampsia
The occurrence of one or more seizures in woman with pre-eclampsia, which is an obstetric emergency
Define HELLP syndrome
Haemolysis, Elevated liver enzymes, and Low Platelets syndrome:
- a severe from of pre-eclampsia that is associated with high maternal and perinatal morbidity and mortality
What causes pre-eclampsia?
Exact mechanism is unclear, but thought to be due to poor placental perfusion:
- The placenta usually invades the spiral arteries of the uterus, causing them to remain dilated and unable to constrict to give a high flow, low resistance circulation
- In pre-eclampsia this remodelling is incomplete, causing a low-flow ureto-placental circulation with high resistance
- The maternal BP rises to compensate for this, and there is also a systemic inflammatory response and endothelial cell dysfunction
What are the risk factors for pre-eclampsia?
High risk:
- hypertensive disease in previous pregnancy
- chronic kidney disease
- chronic hypertension
- diabetes (type 1 or 2)
- autoimmune disease (e.g. SLE, antiphospholipid syndrome)
Moderate risk:
- nulliparity (first pregnancy)
- aged 40 or older
- BMI of 35 or over at first visit
- family history of pre-eclampsia
- multiple pregnancy
- pregnancy interval of more than 10 years
When is prophylaxis for pre-eclampsia indicated?
- Women with 1 high risk factor or 2 or more moderate risk factors
- Aspirin 75mg a day, from 12 weeks gestation until birth
What are the symptoms of pre-eclampsia?
- severe headaches (increasing frequency, unrelieved by regular analgesics)
- visual problems (blurred vision, flashing lights, double vision)
- new persistent epigastric or RUQ pain
- vomiting
- breathlessness
- sudden swelling of face, hands, or feet
What anti-hypertensives are used in pregnancy, and what are their side effects?
- Labetalol (1st line): beta-blocker, avoid in asthma or diabetes, SE = postural hypotension, fatigue, n/v, epigastric pain
- Nifedipine: calcium-channel blocker, SE = peripheral oedema, dizziness, headache
- Methyldopa: alpha-agonist, SE = drowsiness, headache, oedema, bradycardia, postural hypotension, hepatotoxicity, GI upset
** ACEi/ARBs are contra-indicated in pregnancy
What is the management of pre-eclampsia?
- Monitoring (foetal + maternal): blood pressure, urinalysis, blood tests, foetal growth scans, cardiotocography
- VTE prophylaxis: low-molecular weight heparin
- Antihypertensives: labetalol
- Delivery: only definitive cure, decision made on individual basis
What is the inpatient management of severe pre-eclampsia?
- Stabilise blood pressure(labetalol, nifedipine, methyldopa)
- Check bloodsincludingplatelets, renal and liver function (for end-organ damage)
- Magnesium sulphateif applicablee.g.hyperreflexia
- Monitor urine output(fluid restrictto 80mlsper hour)
- Treat coagulation defects
- Foetalwellbeing(CTGs, USS forfoetalgrowth)
- Delivery
What is the management of eclampsia?
- IV MgSo4 4gms given over 5 minutes, followed by aninfusion of 1 g/hour maintained for 24 hours
- May need further doses if recurrent seizures
- Treat hypertensionIV (labetalol , nifedipine , methyldopa,hydralazine)
- Stabilise mother first, then delivery baby
What causes antepartum haemorrhage?
- 40% are unidentifiable cause
- Low lying placenta/placenta praevia
- Vasa praevia
- Minor/major abruption
- Infection
- Trauma/domestic violence
What are the management of antepartum haemorrhage?
- Estimate blood loss: minor (<50ml), major (50-1000ml), massive (>1000 and/pr shock)
- Identify cause: e.g. urgent USS to exclude placenta praevia
- Resuscitation and stabilisation of mother, including blood transfusion if needed (before any decision about baby)
- Do not perform a vaginal examination as this may induce torrential bleeding of placenta praevia
- Foetal monitoring and urgent delivery if foetal distress/compromise
Define placenta praevia
When the placenta has implanted into the lower segment of the uterus, can be major (covering internal os) or minor/partial (in lower segment, encroaching os)
What are the risk factors for placenta praevia?
- High parity
- Maternal age >40
- Multiple pregnancy
- Previous placenta praevia
- Previous C section
- Smoking and cocaine use
- Deficiency in endometrium (e.g. endometriosis, fibroids, previous curettage)
- Assisted conception
What are the clinical features of placenta praevia?
- May present with painless vaginal bleeding, varying from spotting to massive haemorrhage
- May be found incidentally, diagnosed at 20 week USS, repeat scan at 32 and 36 weeks to confirm placenta remains low lying
- Usually no indication of foetal distress unless complications occur
What is the management of placenta praevia?
- Advise patient on high risk of preterm delivery (to present if pain/bleeding, avoid sexual intercourse)
- Antenatal corticosteroid therapy between 34 and 36 weeks
- TVUS at 32 and 36 weeks
- Tocolytics (to prolong gestation)
- Elective C section around 36/37 weeks if asymptomatic, or 34-36 if history of bleeding
Describe vasa praevia
- Foetalvessels coursing through the membranes overthe internal cervicalosand below thefoetalpresenting part, unprotected by placental tissue orthe umbilical cord
- Can present with bleeding, ruptured membranes, foetal bradycardia
- No major maternal risk, but major foetal risk at membrane rupture leads to major foetal haemorrhage
- CTG abnormalities
- Management: elective C section at 37 weeks
Describe morbidly adherent placenta
- When placenta presents through decidua basalis and through myometrium
- Ranging from normal, accreta (at myometrium), increta (in myometrium), and percreta (past myometrium)
- Investigations: UUS (loss of definition of wall of uterus and abnormal vasculature), MRI
- Management: elective C section at 36-37 weeks, conservative method of leaving placenta in place, often hysterectomy, requires lots of blood replacement and ICU care post-op
Describe placental abruption
- Premature separation of the placenta from the uterine wall, partially or completely (before or during labour)
- May or may not have painful PV bleeding (concealed or revealed haemorrhage) depending on location of placenta
- On examination: wood-hard, tense uterus (USS is not reliable)
- Foetal distress (hypoxia leads to heart rate anomalies on CTG)
- Maternal shock may seem out of proportion to bleeding (concealed)
- Management: mother stabilised before decision made about foetus
What are the complications of antepartum haemorrhage?
- Premature labour/delivery
- Need for bloodtransfusion
- Acute tubular necrosis (+/- renal failure)
- DIC
- PPH
- ITUadmission
- ARDS (secondary to transfusion)
- Foetalmorbidity (hypoxia) andmortality
What are the risk factors for maternal sepsis?
- Obesity
- Diabetes
- Impaired immunity
- Anaemia
- Vaginal discharge
- History of pelvic infection
- History of group B Strepinfection
- Amniocentesis and otherinvasive procedures
- Cervical cerclage
- Prolonged spontaneousrupture of membranes
- Group A Strep infection inclose contacts / familymembers
What is the management of maternal sepsis?
Lower threshold for recognition (MEOWS)
Sepsis 6:
- give O2 as required
- give IV antibiotics
- give IV fluids
- take blood culture
- take blood for lactate
- monitor vitals and urine output
Describe cord prolapse
- Occurs after rupturing of the membrane if cord presents first, or alongside presenting part
- Is an obstetric emergency as causes compression or vasospasm of the exposed cord and significant risk of foetal morbidity and mortality from hypoxia
What are the risk factors for cord prolapse?
- Premature rupture membranes
- Polyhydramnios(i.e. a large volume of amnioticfluid)
- Long umbilical cord
- Foetalmalpresentation(e.g. anything but cephalic presentation and longitudinal lie
- Multiparity
- Multiple pregnancy
What is the management of a cord prolapse?
- Call 999(if not in hospital)oremergency buzzer
- Infuse fluid into bladder via catheter if at home
- Trendelenburg position(feet higher than head)
- Constantfoetalmonitoring
- Alleviate pressure on cord
- Emergency C section as soon as possible
Define shoulder dystocia
Failure for the anterior shoulderto pass under the symphysis pubisafter delivery of thefoetalhead
What are the risk factors for shoulder dystocia?
- Macrosomia(large baby, but most cases occur in normally grown babies)
- Maternal diabetes
- Previous shoulder dystocia
- Disproportion between mother andfoetus
- Post-maturityand induction of labour
- Maternal obesity
- Prolonged 1stor 2ndstage of labour
- Instrumental delivery
What is the management of shoulder dystocia?
First line:
- McRoberts position (knees up): often resolves alone
- suprapubic pressure (pressure behind anterior shoulder to disimpact from maternal symphysis)
Second line (after episiotomy):
- rotational manoeuvres
- removal of posterior arm
Third line (rarely used):
- fracture of the foetal clavicle
- symphysiotomy (cutting pubis symphysis)
- Zavanelli manoeuvre (push head back inside and deliver by C section)
Post delivery:
- PR exam to exclude 3rd degree tear
- physiotherapist review of pelvic floor weakness
- paediatric review for complications
What are the complications of shoulder dystocia?
Maternal:
- PPH
- extensive vaginal tear
- psychological
Foetal:
- hypoxia (seizures, cerebral palsy)
- injury to brachial plexus
- humeral fracture
Define post partum haemorrhage
- Primary: within 24 hours
- Secondary: after 24 hours up to 12 weeks
- Minor: 500-1000 mls
- Major: >1000 mls
What are the causes of primary post partum haemorrhage?
4 Ts…
- Tissue: incomplete placenta
- Tone: uterine atony (abnormal contraction following delivery)
- Trauma: peroneal or uterine (due to instrumental delivery, episiotomy, C section
- Thrombin: coagulopathies (DIC, clotting disorders), vascular abnormalities (placental abruption, hypertension)
What are the risk factors for post partum haemorrhage?
- Big baby
- Nulliparity andgrandmultiparity
- Multiple pregnancy
- Precipitate orprolonged labour
- Maternal pyrexia
- Operative delivery
- Shoulder dystocia
- Previous PPH
What is the management of primary post partum haemorrhage?
Treat the cause:
- remove tissue
- repair tear
- improve tone
- treat coagulopathies
Medications:
- sytocinon (synthetic oxytocin to stimulate contraction)
- ergometrine (directly stimulates uterine muscle to contract)
- haemobate (works on prostaglandin receptors to increase contractions)
- tranexamic acid
Surgery:
- balloon tamponade
- haemostatic suture
- uterine or internal iliac artery ligation
- hysterectomy
What are the causes of post-partum haemorrhage?
- 4 T’s:
- Tone (uterine atony)
- Tissue (retained placenta)
- Trauma (perineal/vaginal tear)
- Thrombin (clotting disorder)
Others:
- Uterine infection
- Abnormal involution of placental site
- Trophoblastic disease
What is the management of secondary post partum haemorrhage?
- Resuscitation if needed
- IV antibiotics if infectious cause
- Uterotonics (sytocinon, ergometrine, misoprostol)
- Surgical measures
What does a portogram record?
- Progress of labour
- Foetal condition
- Maternal condition
- Space for drugs, IV, etc.
What does station refer to during labour?
Relationship between the lowest presenting part of baby, and the ischial spine of mothers pelvis
- minus numbers for above, positive for below
- determines delivery: forceps delivery if head is below the spine (if not, needs C section)
Describe the anatomy of the foetal skull
- 4 bones: occipital, temporal, parietal, frontal
- Anterior fontanel: frontal suture, coronal suture, sagittal suture (diamond shaped)
- Posterior fontanel: sagittal suture, lambdoid suture (triangle shape)
What are the diameters of the foetal skull?
- Suboccipital bregmatic: well flexed, 9.5cm
- Occipital frontal: deflexed, 10.5cm
- Mento vertical: extended (brow), 13cm
- Submental bregmatic: hyperextended, 9.5cm
Describe the pain pathway in labour
First stage:
- pain caused by lower uterine and cervical changes
- visceral afferent nerve fibres
- T10-L1
Second stage:
- pain caused from distention of the pelvic floor, vagina, perineum
- somatic nerve fibres, pelvic splanchnic and pudendal nerve
- S2-S4
What are the non-pharmacological managements in labour?
Water:
- helps concentration and relaxation
- works immediately
- make delivery harder for midwife
Sensory methods:
- positioning
- massage
- TENS machine
Phycological:
- relaxation/meditation
- hypnosis
- hypnobirthing
Complementary therapy:
- aromatherapy
- reflexology
- acupuncture
What are the medical forms of pain relief used in labour?
Entonox
- oxygen + nitrous oxide
- pros: fast acting, doesn’t require foetal monitoring
- cons: can cause nausea and dizziness, effect wears off quickly
Opiates
- diamorphine, pethidine, remifentanyl
- pros: still able to mobilise, doesn’t slow down labour, causes drowsiness to help with sleep
- cons: can cause nausea, vomiting, and respiratory distress for mother and baby
Epidural
- bupivacaine + fentanyl administered into epidural space of L3/4
- pros: total relief of pain in most case, patient can control top ups if needed
- cons: loss of mobility and bladder control, can take up to an hour to have effect, can slow down labour
Spinal
- local anaesthetic injected into subarachnoid space into CSF between L3 and 4
- pros: effective total pain relief, suitable for C-section or instrumental delivery
- cons: complications of hypotension, only short lasting
What are the different categories for C section?
- Cat 1: within 30 minutes (emergencies)
- Cat 2: within 75 minutes (foetal distress but not emergency)
- Cat 3: within 24 hours (failed induction)
- Cat 4: elective (planned from clinic)
What hormones are important in labour?
- Oxytocin: surge at onset of labour contracts uterus, stimulated by pressure of baby against cervix
- Prolactin: production of milk in the mammary glands
- Oestrogen: surge at onset of labour inhibits progesterone to prepare smooth muscle for labour
- Prostaglandins: aids cervical ripening (softening)
- Endorphins: natural pain relief, levels rise through labour, but drop with pain medication
- Adrenaline: released when birth is imminent to give the women energy, but can slow labour if too high by causing distress
Describe the pelvic inlet and outlet
Pelvic inlet:
- anterior border: pubic symphysis
- lateral border: iliopectineal line
- posterior border: sacral promontory
- widest diameter: lateral
Pelvic outlet:
- anterior border: pubic arch
- lateral border: ischial tuberosity
- posterior border: tip of coccyx
- widest diameter: anteroposterior
Describe the rupture of membranes
- Can be spontaneous (SROM) or artificial (ARM)
- SROM can happen at any point prior to, or during labour
What is the function of amniotic fluid and sac?
Amniotic fluid acts as a cushion around the foetus, and the foetus also swallows the amniotic fluid which will create urine and meconium
The sac has 2 layers - amnion and chorion (outside)
What blood vessels are in the umbilical cord?
- 1 vein (oxygenated blood and nutrients from placenta to baby)
- 2 arteries (carry waste away from baby)
What are the indications for induction of labour?
- Prolonged gestation (after 40 weeks)
- Premature rupture of membranes (PPROM): after 37 weeks offer IOL after 24 hours, between 34 and 37 timing depends on risks, before 34 weeks delay unless complications
- Maternal health problems: e.g. pre-eclampsia, diabetes, cholestasis
- Foetal growth restriction: to reduce foetal compromise
- Intrauterine foetal death
What are the contraindications of induction of labour?
Absolute:
- cephalopelvic disproportion
- major placenta praevia
- vasa praevia
- cord prolapse
- transverse lie
- previous classical C section
- active primary genital herpes
Relative contraindication:
- breech presentation
- triplet or higher pregnancy
- 2 or more previous low transverse C sections
Describe vaginal prostaglandins for induction of labour?
- First line choice, maximum of 24 hours
- Prostaglandins act to ripen the cervix, and also have a role in contractions of the uterus
- Tablet/gel: 1st does, plus a 2nd dose if labour has not started 6 hours later
- Pessary: 1 dose over 24 hours
Describe amniotomy for induction of labour
- Forewaters are ruptured with an amnihook (artificial rupture of membranes, ARM), only after cervix is ripe
- This process releases prostaglandins to start labour
- Oxytocin infusion (syntocinon) usually started within 2 hours, if labour hasn’t started
Describe membrane sweep for induction of labour
- Classified as adjunct of IOL, increases that likelihood of spontaneous delivery, reduces need for formal induction
- Finger inserted through cervix and rotated against membranes to separate chorionic membrane form decidua
- Helps to release natural prostaglandins and start labour usually within 48 hours
- Usually offered at 40/41 gestation, or before pre-term IOL
Describe cervical ripening balloon for induction of labour
- Mechanical induction using balloon catheter inserted into the vagina above and below the cervix
- Internal pressure increases prostaglandins and oxytocin to ripen cervix and induce labour
What things determine the ripeness of the cervix (Bishop score)?
- Dilation
- Length (effacement)
- Station
- Consistency
- Position
What are the complications of induction of labour?
- Failure of induction: may need C section
- Uterine hyperstimulation: contractions are too long and frequent leading to foetal distress, managed with tocolytic agents
- Cord prolapse: can occur if head is high
- Infection: as more frequent vaginal exams
- Pain: more painful than spontaneous labour
- Uterine rupture: higher risk if previous C section
What are the indications for an instrumental delivery?
- Prolonged second stage (nulliparous = 2hr, multiparous = 1hr)
- Maternal exhaustion
- Maternal medical condition which limits prolonged pushing or exertion (e.g. intracranial pathologies, severe cardiac disease or hypertension)
- Foetal distress
Describe a ventouse delivery
- Cup attached to foetal head via vacuum, over flexion point (midline, 3cm anterior to posterior fontanelle)
- Traction applied perpendicular to cup during uterine contractions
- Associated with more foetal complications, less maternal complications, and lower success rate
Describe a forceps delivery
- Double bladed instrument, different types
- Can be non-rotational (only used when occiput is anterior), or rotational (can rotate mispositioned head before traction is applied)
- Associated with higher risk of maternal complications, lower risk of foetal complications, and higher success rate
What are the pre-requisites for instrumental delivery?
- Fully dilated
- Ruptured membranes
- Cephalic position
- Defined foetal position
- Empty bladder
- Adequate pain relief
- Adequate maternal pelvis
- Foetal head at least at level of ischial spine and no more than 1/5 palpable
What are the contraindications of instrumental delivery?
Absolute:
- unengaged foetal head in singleton
- incompletely dilated cervix in singleton
- true cephalopelvic disproportion
- breech and face presentation (forceps can be used for after-coming head in breech)
- preterm gestation (<34 weeks) for ventouse
- high likelihood of any foetal coagulopathies for ventouse
Relative:
- acute foetal distress with station above level of pelvic floor
- delivery of 2nd twin when head has not quite engaged or cervix reformed
- prolapse of umbilical cord with foetal compromise when cervix is fully dilated and station is mid cavity
What are the complications of instrumental delivery?
Maternal:
- vaginal 3rd/4th degree tears (ventose is x4 and forceps is x10 more likely than normal)
- PPH
- incontinence
- shoulder dystocia
- infection
- VTE
Foetal:
- scalp laceration
- skull fractures
- facial bruising
- facial nerve injury
- cephalhaematoma
- subgaleal haematoma
- retinal haemorrhage
- neonatal jaundice
What are the different types of perineal tear?
- First degree: involving perineal skin only
- Second degree: perineal skin and muscles torn
- Third degree: perineal skin, muscles, and anal sphincter are torn (a: <50% of external, b: >50% of external, c: both internal and external)
- Fourth degree: perineal skin and muscles, and anal sphincter and mucosa are torn
What is the management of perineal tears?
- First degree: heal without treatment
- Second degree: require sutures to repair muscle
- Third and fourth: require specialist repair in theatre
What things dose a CTG monitor?
- Foetal heart rate
- Contractions of the uterus
What are the indications for continuous CTG monitoring in labour?
- Sepsis
- Maternal tachycardia (>120)
- Pre-eclampsia (particularly >160/110)
- Fresh antepartum haemorrhage
- Delay in labour
- Disproportionate maternal pain
- Use of oxytocin
- Significant meconium
What mnemonic is used to assess CTGs?
Dr C BRAVADO
- DR: Define Risk
- C: Contraction
- BRa: Baseline Rate
- V: Variability
- A: Acceleration
- D: Deceleration
- O: Overall
How are contractions analysed on a CTG?
- Used to gauge activity of labour based on the number of contractions in 10 minutes
- Too few = labour is not progressing
- Too many = could indicate uterine hyperstimulation which leads to foetal compromise
How is the baseline rate assessed in a CTG?
- Average foetal heart rate in 10 minute window
- Normal/reassuring: 110-160
- Non-reassuring: 100-109 or 161-180
- Abnormal: below 100 or above 180
What are the causes of foetal tachycardia/bradycardia?
Tachycardia:
- foetal hypoxia
- chorioamnionitis
- hyperthyroidism
- foetal or maternal anaemia
- foetal tachyarrhythmia
Bradycardia:
- postdate gestation
- occiput posterior or transverse presentations
- prolonged cord compression
- cord prolapse
- epidural or spinal anaesthesia
- maternal seizures
- rapid foetal descent
How is variability assessed on a CTG?
- Indicates a healthy foetus that adapts its heart rate in response to change in environment
- Normal/reassuring: 5 - 25
- Non-reassuring: less than 5 for 30-50 mins, more than 25 for 15-20 mins
- Abnormal: less than 5 for over 50 mins, more than 25 for over 25 mins
What are the causes of reduced variability?
- Foetal sleeping (no longer than 40 mins)
- Foetal acidosis due to hypoxia
- Foetal tachycardia
- Drugs (opioids, benzodiazepines, magnesium sulphate)
- Prematurity (<28 weeks gestation)
- Congenital heart abnormalities
Describe accelerations on a CTG
- Defined as an abrupt increase in the baseline foetal heart rate of greater than 15bpm for greater than 15 seconds
- Accelerations occurring alongside uterine contractions is a reassuring sign of a healthy foetus
- The absence of accelerations with an otherwise normal CTG is of uncertain significance
How are decelerations assessed in a CTGs?
- Define as abrupt decrease in the baseline foetal heart rate of greater than 15 bpm for greater than 15 seconds
- Categorised as early, late, variable, and prolonged
Describe early decelerations on a CTG?
- Defined as gradual dips and recoveries in heart rate that correspond with uterine contractions
- Lowest point of declaration corresponds with peak of contraction
- Caused by compression of the foetal head, stimulating the vagus nerve, slowing the heart
- Considered normal and physiological
Describe late decelerations on a CTG
- Gradual falls in the heart rate that start after the uterine contraction
- Lowest point of the deceleration occurs after the peak of the contraction
- Caused by hypoxia in the foetus and can be due to excessive uterine contractions, or maternal hypotension or hypoxia
- Classed as non-reassuring or abnormal
Describe variable decelerations on a CTG
- An abrupt deceleration that may be unrelated to uterine contractions
- Lowest point of the deceleration occurs within 30 seconds and lasts less than 2 minutes
- Often indicates intermittent compression of the umbilical cord causing foetal hypoxia
- Regular variable decelerations are classed as non-reassuring or abnormal
- Accelerations before and after a variable deceleration are known as shouldering, and this is a reassuring sign
Describe prolonged decelerations
- Deceleration lasting more than 2 minutes
- Often indicates compression of the umbilical cord causing foetal hypoxia
- Between 2-3 minutes is classes as non-reassuring, and more than 3 minutes in abnormal
Describe a sinusoidal pattern in a CTG
- Similar pattern to sine wave with smooth regular waves up and down with an amplitude of 5-15bpm
- This is rare but very concerning sign of severe foetal hypoxia, anaemia, or haemorrhage
What are the different categories of the overall impression of a CTG?
- Normal: baseline = 110-160, variability = 5 to 25 bpm, decelerations = none, early, or variable with shouldering for less than 90 mins
- Suspicious: a single non-reassuring factor
- Pathological: two non-reassuring factors, or a single abnormal factor
- Need for urgent intervention: acute bradycardia or prolonged deceleration of more than 3 minutes
What is the rule of 3s for prolonged foetal bradycardia?
- 3 minutes: call for help
- 6 minutes: move to theatre
- 9 minutes: prepare for delivery
- 12 minutes: deliver the baby
What are the risk factors for small for gestational age?
Minor:
- maternal age (>35)
- smoker (1-10/day)
- nulliparity
- BMI <20, or >25
- IVF singleton
- previous pre-eclampsia
- pregnancy intervals (<6 months, >5 years)
- low fruit intake pre-pregnancy
Major:
- maternal age >40
- smoker >11 day
- previous SGA baby
- maternal/paternal SGA
- previous stillbirth
- cocaine use
- daily vigorous exercise
- maternal medical condition
- heavy bleeding
- low PAPP-A
Define intrauterine growth restriction
- When a foetus has failed to reach their own ‘growth potential’
- In utero growth is slowed, and baby may end up ‘small’, but can still be determined ‘normal’ weight but less than expected
What are the risk factors of intrauterine growth restriction?
- Pre-existing maternal disease (e.g. renal, autoimmune)
- Low or high BMI
- Maternal pregnancy complications (e.g. pre-eclampsia)
- IUGR in previous pregnancies
- Multiple pregnancy
- Smoking and drug use
- Infection (e.g. CMV)
- Extreme exercise
- Malnutrition
- Congenital or chromosomal abnormalities
What is the management of intrauterine growth restriction?
- Aim is to prevent in utero demise or neurological damage associated with ongoing placental dysfunction
- Balanced with maximising gestation to avoid complications of prematurity, so management depends on gestation
- Requires repeat scans for growth and amniotic fluid measurements and umbilical artery dopplers
- Indication for emergency C-section = absent or reversed end-diastolic flow
Describe prolonged pregnancy and its risks
- More than 42 weeks gestation
- Common with previous prolonged pregnancies, and nulliparity
- Increased risk of stillbirth, neonatal illness, meconium passage, foetal distress
What is the management of prolonged pregnancies?
- Induction between 41-42 weeks is favoured, despite risk of failure to establish labour
- Cervical sweep usually at 40-41 weeks may help labour start spontaneously
- If patient prefers to wait, offer daily CTGs and deliver by emergency C-section is abnormal
- Associated with increased chances of foetal distress and need for C-section
Define preterm delivery
- Occurs between 24 an 37 weeks gestation
- Highest neonatal risk is before 34 weeks
- Before 24 weeks is considered miscarriage, but some foetuses survive from 22 weeks
- Can be spontaneous or iatrogenic
What are the risk factors for spontaneous preterm labour?
- Previous history
- Extremes of maternal age
- Short interpregnancy interval
- Maternal medical disease (e.g. renal failure, diabetes, thyroid disease)
- Pregnancy complications (e.g. pre-eclampsia, IUGR)
- Male foetal gender
- High haemoglobin
- STIs vaginal infections
- Previous cervical surgery
- Multiple pregnancy
- Uterine abnormalities
- Urinary infections
- Polyhydramnios
- Congenital foetal abnormalities
- Antepartum haemorrhage
- Lower socioeconomic class
What are some methods of prevention of preterm labour?
Cervical cerclage:
- suture in the cervix to strengthen and keep it closed
- can be done electively at 12-14 weeks, or if cervix is short on scanning, or as a rescue even when cervix is dilated
Progesterone supplements:
- pessary from early pregnancy in women at high risk
- prevents cervical softening
Treatment of polyhydramnios:
- reduction of amniotic fluid levels by needle aspiration
- NSAIDs will reduce foetal urine output
What is the management of spontaneous preterm labour?
- Steroids: given between 24 and 34 weeks to promote foetal pulmonary maturity, take 24 hours to act
- Tocolysis: nifedipine or oxytocin receptor antagonists given to delay labour (not stop it), not used for longer than 24 hours
- Detection and prevention of infection: antibiotics if indicated, to reduce maternal and neonatal risks
- Magnesium sulphate: neuroprotective to prevent cerebral palsy, requires monitoring as toxic in overdose
- Transfer: delivery in unit with intensive neonatal care if born <27 weeks or <800g
- Delivery: vaginal is preferred to C-section, with antibiotics due to higher risk of GBS
What are the complications of spontaneous preterm labour?
Foetal:
- need for neonatal intensive care
- cerebral palsy
- perinatal mortality
- chronic lung diseases
- cognitive development problems
Maternal:
- infection
- need for C section
What are the indications for pre-term delivery?
Placental complications:
- placenta praevia
- prior classical c section
- previous uterine rupture
- suspected accreta, increta, or percreta
Foetal complications:
- oligohydramnios
- growth restriction (decreased expected foetal weight and/or abnormal umbilical artery doppler)
- multiple gestations
- autoimmunisation
Maternal complications:
- hypertension/pre-eclampsia/HELLP
- poorly controlled diabetes
- HIV
- obstetric cholestasis
- P-PROM
Define Rhesus haemolytic disease
- If the foetus is D Rhesus positive and the mother is D Rhesus negative, the mother will mount an immune response to create anti-D antibodies (due to a sensitising event)
- In subsequent pregnancies with repeated exposure, large numbers of antibodies will be created and cause immune haemolysis of foetal/neonatal red blood cells
- If mild this leads to neonatal jaundice, or if more severe foetal or neonatal haemolytic anaemia and death
What are potential sensitising events in pregnancy?
An event which can cause a foetomaternal haemorrhage and can result in a pregnant woman becoming sensitised (making an antibody)…
- Termination of pregnancy
- Evacuation of products of conception
- Miscarriage or threatened miscarriage >12 weeks
- Ectopic pregnancy
- Antepartum vaginal bleeding
- Intrauterine death and stillbirth
- Invasive uterine procedure (e.g. amniocentesis)
- External cephalic version
- Abdominal trauma
- Delivery
How is Rhesus disease prevented in pregnancy?
- Giving exogenous anti-D to the mother prevents her creating maternal anti-D and stops immune recognition
- Antenatal anti-D should be given to all Rhesus negative mothers if the foetus is Rhesus positive or unknown at 28 weeks (if not already sensitised)
- Also given antenatally to these women within 72 hours of any sensitising event
- Given postnatally within 72 hours of delivery, along with Kleihauer testing
What is the Kleihauer test?
- Used to screen maternal blood for the presence of foetal red blood cells
- Quantifies the severity of foetomaternal haemorrhage to calculate the dose of anti-D needed
Describe the pathophysiology of diabetes in pregnancy
- Pregnancy is a state of physiological insulin resistance and relative glucose intolerance
- Glucose handling is altered, causing decreased fasting levels and increased levels following a meal
- The glucose tolerance decreases with increasing gestation after the first trimester, due to anti-insulin hormones secreted by the placenta
What are the risk factors for gestational diabetes?
- BMI > 30
- Age > 40
- Black/Asian ethnicity
- Previous gestational diabetes
- 1st degree relative with diabetes
- PCOS
- Previous macrosomia baby (>4.5kg)
- Previous unexplained stillbirth
- Persistent glycosuria
- Polyhydramnios
What are the clinical features and complications of gestational diabetes?
Maternal:
- often asymptomatic, but may diabetic symptoms (polyuria, polydipsia and fatigue)
- increased risk of pre-eclampsia
- worsening of pre-existing ischaemic heart disease
- wound, endometrial, or urinary infections
- more likely to need c section of instrumental delivery
- diabetic nephropathy and retinopathy
Foetal:
- macrosomia (leading to complicated delivery, shoulder dystocia, trauma)
- organomegaly (particularly cardiomegaly)
- polyhydramnios
- increased rates of preterm delivery
- hypoglycaemia after delivery
- Increased risk of perinatal mortality
What investigations are needed for gestational diabetes?
Glucose Tolerance Test (GTT):
- fasting glucose > 5.6mmol/L
- 2 hrs postprandial (75g glucose drink) > 7.8mmol/L
Tested at:
- at 24-28 weeks if risk factors
- earlier (13-14 weeks) if previous gestational diabetes
- at any point of glycosuria
What is the diabetes management of gestational diabetes?
- MDT approach (obstetrician, specialist midwife, dietician)
- Lifestyle advice: diet and exercise (may be sufficient alone)
- Metformin if still raised (or glibenclamide if CI)
- Insulin is still raised, or if fasting glucose >7, pre-meal >6, post-meal >7.5, or foetal abdominal circumference >95th centile)
What is the obstetric management of gestational diabetes?
- Monitoring for pre-eclampsia
- Regular foetal growth scans (usually 28, 32, and 36 weeks)
- Delivery by induction or C section by 40+6 for uncomplicated GDM, or 37/38 for complicated GDM
- Intrapartum foetal monitoring, hourly blood glucose monitoring, insulin infusion if needed
What is the postnatal management of gestational diabetes?
- Stop medication
- Healthy lifestyle advice
- Contraception
- HbA1c at 13 weeks after delivery (if 39-47 at high risk of diabetes, >48 diagnosed with type 2 diabetes)
- Annual HbA1c
What are the effects of pregnancy on pre-existing diabetes?
- Increased insulin dose requirements, particularly in 3rd trimester (T2DM often started on insulin)
- Women with diabetic nephropathy may have deterioration of renal function and worsening proteinuria
- Risk of development or progression of retinopathy
- Hypoglycaemia with relative hypo unawareness
- Diabetic ketoacidosis (risk in hyperemesis, infection, steroid therapy)
What are the risks and complications of pre-existing diabetes in pregnancy?
Maternal:
- miscarriage
- higher risk of pre-eclampsia (increased in hypertension and/or renal disease)
- risk of infection (UTI, respiratory, endometrial, wound)
- increased rate of c section
Foetal:
- congenital abnormalities (neural tube defects, skeletal abnormalities, congenital heart defects)
- perinatal and neonatal mortality
- intrauterine death
- macrosomia (and shoulder dystocia)
- preterm birth (idiopathic or iatrogenic)
- neonatal hypoglycaemia
- respiratory distress syndrome
What is the diabetes management of pre-existing diabetes in pregnancy?
- Monitoring of blood glucose
- Use of continuous glucose monitoring (CGM)
- Provide hypoglycaemia treatment
- Ketone monitoring strips
- Retinal screening (1st trimester, repeated in 3rd trimester if normal)
- Control of existing hypertension
What is the obstetric management of pre-existing diabetes in pregnancy?
- Folic acid 5mg (preconception until 14 weeks)
- Early dating and viability scan
- Aspirin 15-mg once daily from 12 weeks until delivery
- Foetal growth scan at 28, 32, and 36 weeks
- Delivery at 37/38 weeks by induction or C section (sometimes before 37 weeks if complications)
- Intrapartum hourly blood glucose and insulin infusion if needed
What is the post-natal care of pre-existing diabetes?
Maternal:
- insulin doses stopped/returned to pre-pregnancy levels, and adjusted in breastfeeding (increased energy expenditure)
- not as important to have tight glycaemic control
- contraception
- counselling about the importance of planned pregnancy
Neonatal:
- feeding as soon as possible to reduced hypoglycaemia
- blood glucose testing at 2-4 hours after birth
- minimum 24hr hospital stay
Define antepartum haemorrhage
- Bleeding from anywhere within the genital tract after the 24th week of pregnancy
- Occurs in 3-5% of pregnancies
Define obstetric cholestasis
A multifactorial intrahepatic disorder usually developing in the third trimester of pregnancy, commonly presenting with pruritis, elevated levels of bile acid, and/or abnormal LFTs
What are the risk factors for obstetric cholestasis?
- Past history (recur more severely in 50%)
- Family history
- Multiple pregnancy
- Presence of gallstones
- Hepatitis C
What is the presentation of obstetric cholestasis
- Generalised intense pruritis (most common on palms and soles, and worse at night)
- Right upper quadrant pain
- Dark urine and pale stools
- Nausea, anorexia, fatigue
- Clinical jaundice (rare)
What are the investigations needed for cholestasis?
- Total serum bile acid: cut-off value of 10, taken weekly to monitor after diagnosis
- LFTs: particularly ALT may be raised
- Prothrombin time: raised
- US and CTG are not helpful to predict outcomes
What is the management for obstetric cholestasis?
- Ursodeoxycholic acid (relieves pruritis)
- Vitamin K (if prolonged prothrombin time)
- Induction of labour (early if bile acids are very high)
- Follow up 6 weeks postnatal to ensure liver function returns to normal
What are the complications of obstetric cholestasis?
- Increased risk of sudden intrauterine death
- Increased risks during delivery: premature, intrauterine asphyxia, foetal bradycardia,
- Maternal morbidity due to itching and lack of sleep
What are the risk factors for VTE during pregnancy?
Pre-existing factors:
- age > 35
- BMI > 30
- parity > 3
- smoking
- varicose veins
- thrombophilia
- co-morbidities (e.g. cancer)
- family history of unprovoked VTE
Obstetric factors:
- multiple pregnancy
- pre-eclampsia
- prolonged labour
- stillbirth
- preterm birth
- PPH
- use of IVF
Transient factors:
- surgical procedure (except perineal repair)
- dehydration (e.g. hyperemesis)
- ovarian hyperstimulation syndrome
- admission or immobility
- systemic infection
- long distance travel
How is the risk of pregnancy related VTE managed?
Non-pharmacological:
- mobilisation
- hydration
- compression stockings
Low molecular weight heparin:
- antenatal prophylaxis (if high risk)
- postnatal prophylaxis (10 days for lower risk, 6 weeks for higher risk)
- immediate treatment of VTE (stopped before labour)
What is the cause of anaemia during pregnancy?
Disproportionate increase of plasma volume and red blood cell mass, leading to an overall decrease of haemoglobin concentration due to a haemodilution effect
What are the risk factors for anaemia during pregnancy?
- Haemoglobinopathies (thalassaemia, sickle cell disease)
- Increased maternal age
- Anaemia during previous pregnancies
- Poor diet
- Low socioeconomic status
How is anaemia during pregnancy managed?
- Screening of all pregnant women at booking and 28 weeks
- Haemoglobinopathy screening for any confirmed anaemia
- Oral iron supplements (or IV infusion if severe)
- Folate replacement (if indicated)
Define group B streptococcus infection in pregnancy
- GBS is colonised in the vagina or rectum of 25% of pregnant women
- Usually causes no symptoms but can cause sepsis, pneumonia, or meningitis in the neonate
What are the risk factors for group B streptococcus infection in neonates?
- Positive GBS swab in the mother
- UTI caused by GBS in this pregnancy
- GBS infection in previous baby
- Prematurity <37 weeks
- Rupture of membranes >24 hours before delivery
- Pyrexia during labour
How is group B streptococcus infection in pregnancy managed?
- Vaginal or rectal swabs at 35-37 weeks (either as screening or only high risk women)
- Prevention of neonatal infection with high dose IV penicillin during labour
Define hyperemesis gravidarum
Severe and prolonged nausea and vomiting of pregnancy (usually starts between weeks 4-7, peaks at 9 weeks, settles by 20 weeks), leading to weight loss, and dehydration, electrolyte imbalances
What is the pathophysiology of hyperemesis gravidarum?
Rapidly increasing levels of bHCG released by the placenta, which stimulates the chemoreceptors of the brainstem to trigger the vomiting centre of the brain
* hence, multiple pregnancy and trophoblastic disease are risk factors
What are the risk factors for hyperemesis gravidarum?
- First pregnancy
- Previous history
- Raised BMI
- Multiple pregnancy
- Hydatidiform mole
What are the investigations for hyperemesis gravidarum?
- FBC (anaemia, infection)
- U&Es (hypokalaemia, hyponatraemia, renal function)
- Blood glucose (exclude DKA if diabetic)
- Urine dipstick (quantify ketonuria)
- Mid-stream urine (rule out UTI)
- USS (confirm viability and gestation, rule out multiple pregnancy and trophoblastic disease)
What is the management for hyperemesis gravidarum?
- Mild: managed in community, oral antiemetics, hydration, reassurance
- Moderate: managed in day care, IV fluids and antiemetics
- Severe: managed as inpatient, IV fluids and antiemetics, further monitoring
Pharmacology…
- Antiemetics: cyclizine, metoclopramide, ondansetron
- Thiamine: to prevent neurological complications (Wernicke’s encephalopathy) of vitamin depletion
Define oligohydramnios
Low levels of amniotic fluid during pregnancy, defined as being below the 5ht centile for the gestational age
What are the causes of oligohydramnios?
- PPROM (preterm prelabour rupture of membranes)
- Placental insufficiency (causes poor perfusion to foetal kidneys and low urine output)
- Foetal renal abnormalities (renal agenesis, cystic dysplasia, obstructive uropathy)
- Genital/chromosomal anomalies
- Post term pregnancies
- Twin to twin transfusion syndrome (monochorionic twins)
- Maternal causes (dehydration, hypertension, diabetes, hypoxia, viral infection)
How is oligohydramnios assessed?
History:
- symptoms of leaking/feeling damp
Examination:
- symphysis fundal height
- speculum (fluid pooled in vagina)
Ultrasound
- measure liquor volume
- measure foetal size
- look for structural abnormalities
Karyotyping (if appropriate)
What is the management of oligohydramnios?
Caused by ruptured membranes…
- if term, expectant management (labour is likely to begin 24/48 hours after rupture of membranes
- if premature, consider IOL and steroids
Caused by placental insufficiency…
- ongoing antepartum surveillance (foetal growth, liquor volume, umbilical artery dopplers, CTG)
- likely delivery before 36-37 weeks
Others…
- amnioinfusion
- vesico-amniotic shunts
What are the complications of oligohydramnios?
- Potter syndrome
- Pulmonary hypoplasia
- Foetal compression syndrome
- Amniotic band syndrome
- Increased risk of foetal infection
Define polyhydramnios
Abnormally large levels of amniotic fluid during pregnancy, defined as being above the 95th centile for gestational age
What are the causes of polyhydramnios?
- Idiopathic (around 50% of cases)
- Impaired foetal swallowing (oesophageal atresia, CNS abnormalities, muscular dystrophy)
- Duodenal atresia
- Twin to twin transfusion syndrome
- Increased lung secretions
- Maternal diabetes
- Macrosomia
- Multiple pregnancies
- Foetal anaemia
- Foetal hydrops
- Maternal substance misuse
- Genetic or chromosomal abnormalities
How is polyhydramnios assessed?
History:
- excessive maternal breathlessness, early onset of labour or rupture of membranes
Examination:
- tense uterus on palpation
- uterus measures large for dates
- difficulty feeling foetal parts
Ultrasound:
- measure liquor volume
- asses foetal growth and anatomy
- umbilical artery doppler
Others
- maternal glucose tolerance test
- karyotyping (if appropriate)
What is the management for polyhydramnios?
- Induction of labour if foetal distress
- Antenatal corticosteroids (as preterm labour is common)
- Amnioreduction (if maternal symptoms are severe, but risks of infection and placental abruption)
- Indomethacin (prostaglandin synthetase inhibitor, reduces foetal renal blood flow and urine output)
What are the complications of polyhydramnios?
- Preterm delivery
- Placental abruption
- Malpresentation
- Postpartum haemorrhage
- Cord prolapse
Define foetal hydrops
Abnormal fluid accumulation in two or more foetal compartments (abdominal, pleural, skin)
What are the causes of foetal hydrops?
Immune:
- anaemia and haemolysis due to antibodies including rhesus disease
Non-immune:
- chromosomal abnormalities
- structural abnormalities
- cardiac abnormalities
- anaemia (parvovirus infection, foetomaternal haemorrhage, alpha thalassaemia)
- twin-twin transfusion
What investigations are needed for foetal hydrops?
- Detailed ultrasound scans including echocardiogram
- Foetal karyotyping and chromosomal analysis
- Doppler measurements of the middle cerebral artery (to assess anaemia)
- Investigations for maternal-foetal infections
- Testing for alpha thalassaemia if mother at risk
What is the management of foetal hydrops?
Depends on cause:
- antepartum surveillance
- preterm delivery (with corticosteroids)
- intrauterine transfusion to treat anaemia
Many causes are not curable and parents may opt for termination of pregnancy
Describe the different types of prenatal testing for congenital abnormalities
Maternal blood testing (for screening):
- blood markers (bHCG, PAPP-A and alpha fetoprotein) are considered with other risk factors such as maternal age and nuchal translucency
- screens for trisomies 21, 18, and 13
Maternal blood testing (for diagnosis):
- NIPT (non-invasive prenatal testing) uses free foetal DNA in the maternal circulation to diagnose chromosomal abnormalities
- quick and inexpensive, but not 100% accurate
Invasive testing:
- amniocentesis or chronic villus sampling
- samples undergo karyotyping and more detailed chromosomal analysis
- more accurate but risk of miscarriage (1%)
Describe cytomegalovirus in pregnancy?
- Background: type of herpesvirus, 1% of women develop this in pregnancy, 40% transmit to foetus, 10% of infected neonates are symptomatic at birth
- Maternal: usually asymptomatic in immunocompetent, or can cause mild flu
- Foetal: diagnosed by amniocentesis, causes severe problems of IUGR, thrombocytopenia, neurological defects (hearing/vision loss)
- Management: no treatment available, serial USS to assess severity, termination if required
Describe herpes simplex infection in pregnancy
- Background: manifests as cold sores (type 1) and genital herpes (type 2), vertical spread is common in vaginal delivery following recent maternal infection
- Foetal: neonate infection is rare but has a high mortality
- Management: C section if genital lesions present or within 6 weeks of primary infection, maternal acyclovir in late pregnancy to reduce chance of recurrence, neonatal acyclovir if exposed
Describe varicella/herpes zoster virus infection in pregnancy
- Background: primary infection of varicella zoster virus causes chicken pox and reactivation causes shingles
- Maternal: if not previously exposed and immune, chickenpox in pregnancy can cause severe maternal illness including pneumonia, neurological complications, haematological rash
- Foetal: infection in late pregnancy is usually asymptomatic, but in early pregnancy it can cause skin scarring, eye defects, hypoplasia of limbs, neurological defects and rarely teratogenic
- Management: in non-immune mothers, varicella zoster immunoglobulin to prevent and acyclovir to treat, neonatal acyclovir if needed
Describe rubella infection in pregnancy
- Background: usually affects children with mild illness and macular rash, but congenital rubella is rare due to widespread vaccination
- Maternal: often asymptomatic, or non-specific with fine rash, self limiting and no treatment
- Foetal: severe malformations including deafness, cardiac defects, CNS abnormalities are very common (90%) before 12 weeks, but less common as gestation increases
- Management: maternal screening, termination is appropriate with early gestation, close monitoring with later gestations
Describe parvovirus B19 infection in pregnancy
- Background: 50% of women are immune, but if infected causes ‘slapped cheek’ usually caught from children
- Maternal: mild self-limiting illness, usually asymptomatic but can cause symmetrical arthralgia in adults
- Foetal: causes anaemia, foetal hydrops, and sudden intrauterine death (approx. 9% of infected pregnancies)
- Management: serial USS and doppler assessment, in utero transfusion if severe anaemia
Describe hepatitis infection in pregnancy
- Background: hep B and C are spread through blood products and sexual contact, risk factors include drug abuse and being HIV positive
- Maternal: 10% of infected women will be chronic carries of hep B, but 80% for hep C
- Foetal: vertical transmission of hep B occurs in 90% of neonates, but only 3-5% for hep C
- Management: routine maternal screening and neonatal immunisation for hep B, screening for hep C in high risk groups only
Describe HIV infection in pregnancy
- Background: risk of vertical transmission during delivery or breastfeeding in 15% without preventative measures, and is greater with low CD4 count and high viral load
- Maternal: may increase risk of pre-eclampsia and gestational diabetes
- Foetal: risks of stillbirth, growth restriction, and prematurity, 25% of infected neonates develop AIDS by 1 year
- Management: routine maternal screening, maternal and foetal antiretroviral therapy, elective caesarean section, avoidance of breastfeeding
Describe chlamydia in pregnancy
- Chlamydia during pregnancy can ascend from the vagina and cause chorioamnionitis, which can lead to early rupture of membranes and premature delivery
- If a baby is born vaginally while mother has an active infection of chlamydia, neonatal complications include conjunctivitis and pneumonia
Describe syphilis in pregnancy
- 25% of pregnancies to mothers with untreated syphilis result in 2nd trimester miscarriages or stillbirths
- 70-100% of infants born to mothers with untreated early syphilis will be infected
- Symptoms of congenital syphilis include a rash, hepatosplenomegaly, skeletal deformities, lymphadenopathy, deafness
Describe neural tube defects
- Results from the failure of the neural tube, often exposing neural tissue
- Most common are spina bifida (causes severe to mild disability) and anencephaly (incompatible with life)
- All women should take preconceptual folic acid supplements (0.4mg/day)
- Can recur in 1 in 10 future pregnancies but this risk is reduced by high dose folic acid (5mg)
Describe abdominal wall defects
- Exomphalos: abdominal contents herniate through umbilical cord covered by a thin membrane, often associated with chromosomal disorders (50%)
- Gastroschisis: abdominal contents herniate into the amniotic sac with free loops of bowels in the amniotic cavity, rarely associated with other abnormalities
Describe urinary infections in pregnancy?
- Urine infection is associated with preterm labour, anaemia, and perinatal morbidity and mortality
- Urine is dipped regularly and is cultured at booking for asymptomatic bacteriuria which in pregnancy is more likely to lead to pyelonephritis
- Treat with antibiotics: nitrofurantoin is first line (except at term as risk of neonatal haemolysis), not trimethoprim in first trimester or folate deficient
Describe the risks of obesity in pregnancy
- Maternal: higher risk of VTE, pre-eclampsia, diabetes, caesarean section, PPH
- Foetal: higher rate of congenital abnormalities, and perinatal mortality due to pre-eclampsia and diabetes
- Management: preconceptual weight loss, but weight is best maintained during pregnancy, screening for GDM, closer blood pressure surveillance, anaesthetic risk assessment, VTE prophylaxis
Describe sickle cell disease in pregnancy
- Background: recessive disorder due to abnormal beta-chain formation as an S chain, resulting in abnormal haemoglobin
- Maternal: acute painful crises, pre-eclampsia, thrombosis
- Foetal: miscarriage, IUGR, preterm labour, mortality
- Management: ensure adequate hydration, stopping hydroxycarbamide as teratogenic, aspirin and VTE prophylaxis
Describe antiphospholipid syndrome in pregnancy
- Presence of lupus anticoagulant and/or anticardiolipin antibodies
- Results in thrombotic events, which lead to recurrent miscarriages, IUGR, pre-eclampsia
What are the different types of multiple pregnancies?
- Dizygotic twins (2/3 of all multiple pregnancies) or triplets: fertilisation of different oocytes by different sperm
- Monozygotic twins: mitotic division of a singe zygote, which can share the same amnion and/or placenta (dichorionic diamniotic = own amnion and placenta, monochorionic diamniotic = separate amnions but shared placenta, monochorionic monoamniotic = shared amnion and placenta)
What are the complications of multiple pregnancies?
- Maternal: increased risk of gestational diabetes, pre-eclampsia, anaemia, hyperemesis gravidarum
- All multiples: increased risk of IUGR, preterm delivery, miscarriage, congenital abnormalities, malpresentation
- Monochorionic (shared placenta): twin-twin transfusion syndrome (unequal blood distribution, with one twin depleted and one overloaded), IUGR, anaemia, co-twin death
What is the management of multiple pregnancies?
- Early diagnosis and identification of chronicity
- Increased surveillance for pre-eclampsia, diabetes, anaemia
- Serial USS, especially for twin-twin transfusion or IUGR
- Delivery at 36-37 weeks, caesarean if first twin is not cephalic
