Obs - Labour and Birth Flashcards

1
Q

How would you take an Obstetric history?

A
FRAB
Foetal Movements
Rupture of membranes - if occurred, colour (if meconium stained e.g.)
Abdominal pain
Bleeding

+ SR (Headaches, nausea/vomiting, vision changes, SOB, itching etc)

Also:

  • Current pregnancy - gestation, EDD, gravity and parity + any plans for delivery
  • Previous pregnancies - outcomes, modes of delivery, complications and antenatal conditions, BW of babies
  • Hx of diabetes, pre-eclampsia and FHx, cancers/abnormal smears
  • PMH and DHx important e.g. epilepsy, DM, chronic conditions
  • Gynae Hx - cancers/abnormal smears
  • BLOOD GROUP (i.e. Rh status)
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2
Q

What is normal labour defined as and what is the epidemiology of modes of delivery? What is a common DDx?

A

Labour = painful uterine contractions –> cervical effacement and dilation

600,000 babies born/year

  • 60% natural (inc induction)
  • 30% C-section
  • 10% instrumental

Braxton-Hicks = not true labour contractions, may be painless and NO cervical changes

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3
Q

What is cervical cerclage?

A

IF someone’s cervix is dilating due to cervical insufficiency then you may perform cervical cerclage (a band/stitch to keep the cervix closed until labour)

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4
Q

What are the 3 stages of labour?

A

1st stage: from the start of painful uterine contractions until the cervix is fully dilated (10cm). May take many hours (12-20h*)
> Latent 1st –> begins with painful, irregular contractions, cervix dilates from 0-3cm
> Active/Established 1st –> Regular painful contractions, 4/+cm - 10cm

2nd stage: starts with the urge to push and ends with the delivery of the foetus
> Analgesia (‘1,2,3 and analgesia = +1h)
–> In nulliparous women = 3h with epidural or 2h with no epidural
–> In multiparous women = 2h with epidural or 1h with no epidural

3rd stage: delivery of the placenta and foetal membranes, may last up to 30 mins

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5
Q

What is the progress of labour dependent on?

A

3 Ps:
Power - of contractions
Passenger - diameter of foetal head
Passage - dimensions of pelvis

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6
Q

What are the stages of baby delivery: [see pic for help]?

A
  1. Head floating, before engagement*
  2. Engagement, flexion and descent
  3. Further descent and internal rotation (face toward mothers spine)
  4. Complete rotation, beginning extension
  5. Complete extension - head is emerging from the vaginal canal
  6. Restitution (external rotation - bringing the head in line with the shoulders)
  7. Delivery of anterior shoulder
  8. Delivery of posterior shoulder

FROM TUTORIAL:

  1. Baby is OT (occiput-transverse) at entry to the pelvic floor
  2. Head is flexed to enable smallest head diameter
  3. Rotation to OA to enable exit from pelvic outlet and descent down
  4. Head extension to enable delivery
  5. Restitution = rotates back to OT to enable shoulder exit from the pelvic outlet and delivery

The changes in denominator position enable the baby to fit through the widest parts of the pelvis.

*engagement = when widest part of foetal head passes through the widest part of the maternal pelvis successfully

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7
Q

What is the Bishop’s score? What do the scores indicate?

A

A score used to estimate how likely one is to go into labour soon. 5 parameters:

Cervical position - 0->1->2 (posterior, intermediate, anterior, -)

Cervical consistency - 0->1->2 (firm, intermediate, soft, -)

Cervical effacement - 0->1->2->3 (0-30%, 40-50%, 60-70%, 80%)

Cervical dilation - 0->1->2->3
(<1cm, 1-2cm, 3-4cm, >5cm)

Foetal station* - 0->1->2->3
(-3, -2, -1,0 and +1,+2)

*Position of baby’s head relative to maternal ischial spines

Scores: (0-13)
<3 - IOL unlikely to be successful
5 or less - IOL with PV prostaglandin gel should start labour or ripen cervix
–> [<5 = unlikely spontaneous labour]
6-8 - ARM or artificial rupture of membranes (amniotomy +/- oxytocin infusion if labour doesn’t begin)
9/+ - labour likely to occur spontaneously

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8
Q

How would you manage stage 1 of labour? What is classified as ‘delay’ and what are some types/causes?

A

Mx:

  • 1:1 midwifery care
  • Vaginal examinations 4-hourly or as clinically indicated
  • Labour progress is monitored using a partogram:
  • –> normal progress = ~1cm/hour (a well-flexed head will speed this up)
  • –> delay* = <2cm over 4h
  • Adequate analgesia +/- antacids and hydration and light diet to prevent ketosis, which can impair uterine contractility
  • Note: membrane may be ruptured or intact at this stage

Latent 1st phase

  • > Mobilise and managed away from the labour suite (standing may encourage process of labour)
  • > Avoid intervention
  • Delay
  • If membranes intact then initiate ARM and review in 2h
  • If membranes ruptured, give oxytocin, increasing every 15-30mins until contractions are regular. Once regular, review 4-hourly

Types:

  • Primary dysfunctional labour = <2cm dilation in 2h, never progressed properly, most commonly due to ineffective uterine action
  • Secondary arrest of labour (progressed well, then stopped)
  • Prolonged latent phase
  • Cervical dystocia - rare, where cervix doesn’t dilate properly
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9
Q

How would you manage the 2nd stage of labour? What is classed as a delay? What is crowning?

A

First sign of 2nd stage is the URGE to PUSH (w 10cm dilation)

  • > Full dilation confirmed by vaginal examination, if head is not visible
  • > Women should be discouraged from lying supine or semi-supine
  • > Use of epidural/spinal anaesthesia may interfere with the normal urge to push, therefore 2nd stage is usually diagnosed with routine scheduled vaginal examination

Passive 1st stage:

  • No pushing
  • Eg. if Epidural in, then 1h wait

Delay/Prolonged 2nd stage:

  • > In nulliparous women normally takes 2h or 3h with epidural
  • > In multiparous women, takes 1h or 2h with epidural
  • Longer than 1/2h (depending on parity) = delay
  • If membranes intact, initiate ARM and review in 2h
  • If ruptured, give syntocinon and then review 4-hourly
  • If no progress, then consider instrumental delivery

Delivery:

  • > Watch the perineum - between contractions, the elastic tone of the perineal muscles will push the head back into the pelvic cavity -> when head no longer recedes between contractions = CROWNING and indicates delivery is imminent
  • > As crowning occurs, hands of the midwife are used to flex the foetal head and guard the perineum
  • > Once the head has crowned, the mother should be discouraged from bearing down by telling her to take rapid, shallow breaths
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10
Q

What is done in the immediate care of the neonate?

A
  • Baby takes first breath within seconds
  • No need for immediate clamping
  • Once cord is clamped, the baby is dried and then has its APGAR score calculated at 1 and 5 mins (>7 is normal) + VitK injection given in delivery room also
  • Immediate skin-skin contact helps oxytocin release and bonding
  • Initiation of breast feeding should be done in 1st hour of life, followed by routine measurements (HC, weight, temperature)
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11
Q

What are the causes of postpartum haemorrhage?

A
4 Ts:
Tone - uterine atony (commonest = 70%)
Trauma - laceration (20%)
Tissue - retained products (10%)
Thrombin - coagulopathy (1%)
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12
Q

How is the 3rd stage of labour managed?

A

Mx:

  • Expulsion of placenta and foetal membranes
  • Normally takes 5-10 mins
  • Mx can be described as active or physiological

Active Mx: [recommended to all women]

  • 10 IU oxytocin IM/ ergometrine (only oxytocin if hypertensive) - given on anterior shoulder immediately after delivery and before the cord is clamped and cut
  • Cord clamped after 1-5 mins
  • Use controlled cord traction to remove the placenta
  • -> signs of placental separation = gush of blood, cord lengthening, uterus becomes round and uterus rises
  • -> Uterine inversion is a rare complication
  • -> IF no bleeding occurs, attempt again after 10 mins (2% cases have failure of this method)
  • Prolonged 3rd stage defined as >30 mins for active Mx and >60 mins for physiological (move to active after this)

Physiological management:

  • Placenta is delivered by maternal effort with no uterotonic drugs
  • Associated with more bleeding and greater need for blood transfusions
  • If haemorrhage occurs or placenta undelivered after 60 mins then active Mx recommended
  • If retained, examination under anaesthesia and MROP

Post-delivery

  • Inspect placenta for missing cotyledons and succenturiate lobe
  • Inspect vulva for tears
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13
Q

How is labour induced?

A

IOL:

1st - Membrane sweeping

  • > Offered prior to formal induction
  • > Repeat if labour not starting
  • > Nulliparous women - offer at 40-41 weeks, Multiparous - offer at 41w

2nd - Prepare the cervix with prostaglandins (E2)

  • > Preferred formal method of induction
  • > Gel, tablet (1 dose followed by 2nd dose after 6h) OR pessary* (1 dose over 24h)
  • > MAX 2 doses
  • > Risk of uterine hyperstimulation
  • > In cases of intrauterine foetal death, misoprostol and mifepristone may be used instead

3rd - ARM

  • > Artificial rupture of membranes i.e. amniohook
  • > NOT first line

4th - Syntocinon (synthetic oxytocin IV)

5th - CS

SUMMARY*:
Order: Propess –> Prostin if insufficient pessary, max 2x 6-hourly –> ARM –> Syntocinon –> CS

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14
Q

When might IOL be indicated? And when might it NOT?

A

IOL indications:

  • > Prolonged pregnancy (from 41w) - if declined, twice weekly USS and CTG
  • > Maternal request in exceptional circumstances, considered at 40w/after
  • > IU foetal death - offered if membranes intact but indicated if ruptured membranes, infection or bleeding (induced with oral mifepristone and then pristine/misoprostol)

-> Previous CS - use pristine/propess but increases risk of uterine rupture and need for a second CS

NOT indicated:

  • > PPROM (pre-term pre-labour rupture of membranes) - avoid induction before 34w; after 34w use prostin/propess but be aware of infection risk
  • > Breech/transverse lie - not recommended (only consider if CS and ECV declined or unsuccessful)
  • > severe IUGR - CS indicated
  • > Suspected foetal macrosomia
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15
Q

What analgesia is used in labour?

A

Non-pharmacological:

  • TENS
  • Breathing techniques
  • Massages

Pharmacological:

  • Paracetamol, codeine
  • Entonox (50% NO in O2): SE = nausea, light-headed, dry mouth
  • Meperidine (pethidine, IM 1mg/kg): SE = ‘sleepy baby’, low baby RR, constipation
  • Morphine (0.1-0.15mg/kg) or Diamorphine (5-7.5mg IM): SE = ‘sleepy baby’, low baby RR, constipation
  • Fentanyl PCA 20microgram bolus with 5 min lockout: SE = ‘sleepy baby’, low baby RR, constipation

Surgical: [later stages]

  • SE = slow labour, increased instrumental risk
  • Lumbar epidural [bupivacaine, ropivacaine, levobupivacaine, chloroprocaine]
  • Combined lumbar-spinal epidural [fentanyl 10-25mcg ± bupivacaine 2.5mg]
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16
Q

What is puerperal pyrexia? How is it caused and managed?

A

Puerperal pyrexia = fever >38 in first 14d following delivery

Causes = ENDOMETRITIS&raquo_space;> UTI, VTE, mastitis, wound infection

Mx - until fever has reduced for at least 24h
-> IV Clindamycin AND IV gentamicin

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17
Q

How is LGA defined? What 3 tools can be used prenatally to determine this?

A

LGA is used to define macrocosmic babies, usually 4 or 4.5kg and above at term
-> 10% pregnancies

3 tools:

  • Symphysis-Fundal height (SMH) - >90/95th centile for GA (foetal biometry)
  • Abdominal circumference - >90/95th centile for GA
  • Estimated foetal weight - > >90/95th centile for GA
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18
Q

What are some RFs for LGA?

A

Main RFs:

  • High BMI/Obesity
  • Gestational or DM

Others:

  • Multiparity
  • Polyhydramnios
  • Advanced maternal age
  • Molar pregnancy
  • Syndromes e.g. Soto’s, Beckwith-Wiedmann
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19
Q

How would a baby LGA present? What Ix would you consider?

A

On inspection - excessive distension for GA
Abdomen - increased SFH, increased abdominal circumference

Ix:

  • OGTT for gestational diabetes
  • Bloods -> serum BHCG
  • USS - liquor volume, biometry
  • Genetic testing
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20
Q

How would you manage a baby LGA? (hint: depends on when detected)

A

Detected at 18-21w
- Repeat scan

Detected at 24-36w

  • If acceleration of growth, arrange a USS for foetal biometry
  • If no drop/rise growth then reassure this is normal and arrange another routine scan
  • Offer OGTT for GD

Detected at 36-40w

  • If SFH is >90th centile on routine measurements, arrange for USS for foetal biometry
  • If EFW and AC on USS are >95th centile, then return to routine care
  • Perform OGTT for GD
  • Care in labour + postnatally as per GD Dx at earlier gestation

Note: need to plan delivery and discuss risks (shoulder dystocia, nerve injuries, prolonged labour) –> Offer CS

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21
Q

What are some complications of LGA babies?

A
  • Shoulder dystocia
  • Hypoglycaemia in GDM
  • Respiratory distress syndrome (due to GDM + need of earlier delivery)
  • Intrauterine deformations (metatarsus adductus, hip subluxation)
  • Perineal tear
  • Increased mortality

But prognosis is good/indifferent to normal babies if detected and managed earlier

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22
Q

How is a baby SGA defined? What is the difference between IUGR and SGA? What are some RFs for SGA?

A

SGA - derived from birth weight –> describes a baby with AC or EFW in the 10th or lower centile for GA
-> 5% pregnancies

IUGR - derived from growth rate –> a baby with a reduced growth rate and so becomes SGA

RFs:
Major: [Maternal] 
-> Previous still birth
-> Antiphospholipid syndrome
-> Renal disease
-> Maternal age >40
-> Smoker >11 cigs/day
Major: [Foetal/other]
-> Chromosomal abnormalities (symmetrical IUGR)
-> Infection (CMV, rubella)
-> Multiple pregnancy
-> Placental insufficiency (asymmetrical IUGR - normal head, but AC and peripheries smaller)

Minor: [See RCOG for full list]

  • Maternal age >35
  • Nulliparity
  • BMI <20 or 25-34.9
  • Smoker 1-10 cigs/day
  • IVF singleton pregnancy
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23
Q

How would you Ix a baby SGA?

A

Ix:

  • > Assess RFs at booking visit (1st trimester)
  • If 1/+ major RF or 3/+ minor RFs then reassess at 20w
  • At 20w and still at risk, consider:
  • > Minor risk (3/+ minor RFs) = uterine artery doppler (20-24w) and if abnormal –> serial USS from 26-28w
  • > Major risk (1/+ major RFs) = foetal size and umbilical artery doppler (serial USS from 26-28w)
  • > Screen for congenital infections

IF SGA or IUGR:
-> USS biometry (biparietal diameter, HC, AC and femur length) and UMBILICAL ARTERY doppler serial measurements should be taken (every TWO weeks)

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24
Q

How would you manage SGA baby?

A

Mx:

  • Stop smoking, drugs and alcohol
  • [Low dose aspirin may be used in preventing IUGR in high-risk pregnancies, NOT reversing however]

Monitoring:

  1. SFH or risk status determined at booking or antenatal appointment
  2. Confirm SGA with foetal biometry (20w)
  3. Uterine artery doppler (20-24w)
    - -> Normal = repeat scans every 2w from 20-24w
    - -> Abnormal = serial growth scans every week from 26-28w and doppler USS can be performed 2x/week (umbilical artery flow)

Delivery:

  • IMMEDIATE delivery indications = abnormal CTG (+reduced foetal movements) and reversal of end-diastolic flow of umbilical artery (placental insufficiency)
  • Delivery by 37w is usually necessary depending on severity and gestation
  • –> steroids given <36w
  • –> Consultant led clinics and decision making
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25
Q

What are some complications of SGA babies? What is their prognosis?

A

Complications:

  • Stillbirth
  • Post-natal hypoglycaemia
  • Birth asphyxia
  • Intrapartum foetal distress
  • Pre-term labour
  • Neurodevelopmental delay

Prognosis - increased perinatal morbidity, increased neurodevelopmental delay if onset <26w

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26
Q

What is the difference between PROM and PPROM?

A

PROM = Pre-labour rupture of membranes

  • Spontaneous rupture of membranes before labour at TERM (37w/+)
  • Occurs in <10% women
  • Natural physiological cause e.g. Braxton-Hicks contractions and cervical ripening –> weakened membranes

PPROM = pre-term pre-labour rupture of membranes

  • Spontaneous rupture of membranes before onset of labour in pregnancy from 24+0w to 36+6w
  • Occurs in 2% pregnancies
  • Can be caused by weakened membranes from infective cause
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27
Q

How may PROM/PPROM present? How would you Ix this?

A

Sx:

  • PROM vs PPROM depends on whether pregnancy is at term
  • Sudden gush of fluid PV -> constant trickle
  • Contractions - if regular and painful then PTL, if not BH
  • General examination - assess for signs of infection such as tachycardia or fever

Ix:
1st = Speculum
-> Amniotic fluid pooling is diagnostic of P/PROM - also the Os may be open or closed
-> If no pooling, test IGFBP-1 or PAMG-1
-> Do NOT use KY jelly as will complicate FFN result
-> Only perform if ROM isn’t evident
-> DO NOT do bimanual as increases infection risk

If >30w, contractions present and Os closed then do
= TVUSS for cervical length
- <15mm is likely to be PTL
- >15mm is unlikely to be PTL

Do not perform diagnostic tests for PPROM if labour becomes established - i.e. bulging membranes, abdominal pain, in a women presenting suggestive of PPROM -> ADMIT to labour ward

2nd = IGFBP-1 (insulin growth factor binding protein 1) or PAMG-1 (AKA Partosure = placental alpha-microglobulin 1)

3rd = FFN + (foetal fibronectin) from gestational sac MAY be detectable
- <24w and >34w would be detectable, and + in PPROM but not detectable in 24-34w

Mx: as per rupture of membranes i.e. not ruptured = PTL and ruptured = PROM/PPROM

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28
Q

How is PROM and PPROM managed? What are RFs for each? What are complications of each?

A

RFs = APH, previous PROM/PTL, smoking, trauma, UTI, multiple pregnancy, uterine abnormalities, cervical incompetence

PPROM
Mx:
- ADMIT and expectant management until 37w if no complications
- Erythromycin for 10d/until labour established
- CS if <34w
- MgSO4 if <30w OR in labour OR planned birth in <24h
- Regular assessment with clinical assessment, bloods and CTG

Risks = maternal sepsis, cord abruption, foetal death, prematurity, cord prolapse
PROM:
- if <24h then expectant management, most women go into labour within 24h
- >24h then IOL - 4-hourly temperature and 24h foetal monitoring; augment with prostaglandin or oxytocin infusion
OR
- Meconium seen - induce labour ASAP

PACES advice:

  • 60% women go into labour within 24h, but will attempt to induce after 24h
  • Risk of neonatal infection if slightly raised (1% vs 0.5% for intact membranes)
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29
Q

What is the definition of PTL, very PTL and extremely PTL? What are the causes of PTL?

A

Pre-term labour is when labour occurs at 32-37w GA

Very PTL = labour 28-32w GA

Extremely PTL = labour at <28w
-> 24w is seen as the limit of viability (55% survival)

Causes of PTL:

  • Infection (20-40%)
  • Uterine abnormalities
  • Cervical procedures
  • Overdistension of the uterus i.e. multiple pregnancy, polyhydramnios
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30
Q

What are RFs for PTL?

A

RFs:

  • Previous PTL/PROM/PPROM
  • Miscarriage at 16-24w
  • Cervical biopsy
  • INFECTION
  • Structural - uterine abnormalities, pre-eclampsia
  • Mechanical - stretch
  • Smoking, high BMI, drugs, extreme ages
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31
Q

How would you Ix and Mx PTL? What are complications of PTL?

A

Ix:

  • > Abdo exam
  • > Speculum
  • > TVUSS if Os closed
  • > CTG monitor
  • > Urine dip +/- MC&S if indicated

Mx:
[Note: Ruptured membranes = PPROM guidance]

Non-ruptured membranes:
-> Tocolysis if 34w (1st=Nifedipine, 2nd=Atosiban)
-> Corticosteriods if 34w for 24h (+insulin in diabetics)
-> MgSO4 for 30w; labour OR planned birth <24h
-> Surgical = emergency ‘rescue’ cerclage indicated if 16-28w, dilated cervix and exposed UNRUPTURED membranes however is contraindicated in infection, bleeding and uterine contractions
-> Prophylactic vaginal progesterone (16-24w) / cervical cerclage offered to women:
 History of PTL (<34w GA) AND cervical length <25mm
 History of >16w GA miscarriage AND cervical length <25mm
 Cervical length <25mm AND history of PPROM
 Cervical length <25mm AND cervical trauma

Complications:

  • Preterm birth complications = ‘big 4’:
  • -> RDS (of which O2 treatment can also cause ROP)
  • -> NEC
  • -> IVH
  • -> Periventricular leukomalacia (PVL)
  • Sepsis
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32
Q

What is a hydatiform mole? What is it caused by and what are RFs associated with it?

A

A benign tumour of the trophoblastic tissue due to abnormal fertilisation leading to formation of a ‘mole’:

  • Complete mole = empty ovum fertilised by either 2 sperm, or 1 sperm which duplicates its DNA (46XY or 46XX)
  • Partial mole = normal ovum (1 set maternal chromosomes) fertilised by 2 sperm, or 1 sperm which duplicates its DNA (69XXY or 69 XXX)

RFs:

  • Extremes of reproductive age
  • Previous GTD
  • Diet - low beta carotene, low saturated fat
  • Ethnicity - Japanese, asians, native Americans
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33
Q

How may a pregnant lady present with a molar pregnancy?

A

Sx:

  • Large for GA (e.g. SFH)
  • Painless PV bleeding (i.e. miscarriage)
  • Hyperemesis from elevated bHCG
  • Symptoms of hyperthyroidism (rare, due to bHCG mimicking TSH)
  • [Often seen on USS before symptoms]
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34
Q

How would you Ix a suspected molar pregnancy?

A

Ix:

  • Bloods - grossly elevated bHCG, low TSH and high T4 due to mimicking by bHCG
  • Pelvic USS
  • -> Complete mole = ‘snowstorm’ appearance, ‘cluster of grapes’, no foetal parrts
  • -> Partial mole = foetal parts seen, NO snowstorm or ‘cluster of grapes’
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35
Q

How would you manage a molar pregnancy?

A

Mx:

  • Urgent referral to a specialist centre for GTD
  • Surgical management using ERPC (evacuation of retained products of conception)
  • Monitoring - serial bHCG monitoring in specialist centre, given methotrexate if rising/stagnant levels and avoid pregnancy until 6m of normal levels
  • Advice
  • -> NO conceiving until f/u complete (use barrier and COCP)
  • -> Avoid IUDs until HCG normalised
  • -> If continues to rise, query choriocarcinoma?
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36
Q

What are complications of a molar pregnancy? What is the risk of recurrence?

A
  • Can progress to malignancy (20% complex moles, 2% partial moles)
  • Partial mole has 0% risk to choriocarcinoma
  • Complete mole has 10% risk of invasive mole and 2.5% risk choriocarcinoma
  • Recurrence risk 1%, if 2/+ molar pregnancies then rises to 17%
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37
Q

How would you counsel someone (PACES) on a molar pregnancy?

A

Counselling: = breaking bad news

  • Explain Dx - foetus doesn’t form properly and baby doesn’t develop but instead an irregular mass of tissue is produced
  • Pregnancy is not viable
  • Explain risks - can invade and damage other tissues
  • Explain management - immediately refer you to specialists and they will surgically manage by removing the mass under GA
  • Explain need for follow up, specialists will see you after, check your bloods to make sure your pregnancy hormone, which is overproduced in molar pregnancy, is coming down
  • Future pregnancy - this doesn’t affect your fertility but 1%/1 in 80 chance of recurrence, but we ask to wait 12m until trying again and ensure follow up is complete and normal
  • RFs if present - advanced maternal age/<20y, previous molar pregnancy, prior miscarriages, asian heritage
38
Q

What are the forms of GTD malignancy? What are the causes of it and what are some RFs associated?

A

GTD malignancy is a form of GTD associated with local invasion or metastasis

  • 1/20-30,000 pregnancies
  • Rapidly metastasising - lung, vagina, brain, liver, kidney

Forms:

  • Invasive mole –> hydatiform mole with invasion of myometrium, necrosis ad haemorrhage
  • Choriocarcinoma –> cytotrophoblast and synctyiotrophoblast without formed chorionic villi invade myometrium and rapidly metastasise
  • Placental site trophoblastic tumour –> intermediate trophoblasts infiltrate myometrium without causing destruction, very rare (<1% GTD)

RFs

  • Extremes of reproductive age
  • Ethnicity
  • Diet
  • Previous GTD

Caused by abnormal chromosomal material of placental tissue

  • Invasive moles ALWAYS follow hydatiform mole
  • Choriocarcinoma arises from molar pregnancy (50%), viable pregnancies (22%), miscarriages (25%) and rarely, ectopic pregnancies (3%)
39
Q

How may a patient present with GTD malignancies?

A

Sx:

  • Persistent PV bleeding
  • Hyperemesis gravidarum
  • Lower abdominal pain
  • Lung metastasis - haemoptysis, dyspnoea, pleuritic pain
  • Bladder and bowel metastasis - haematuria, PR bleeding
  • LARGE FOR GA
40
Q

How would you Ix and manage GTD malignancy? What are complications of it?

A

Ix:

  • Serum bHCG grossly elevated on bloods + LFTs, FBC, U&Es for mets
  • Pelvic USS - ‘snowstorm’, vesicles or cysts
  • Other imaging for metastasis –> CXR, CT CAP, MRI brain

Mx:

  • Managed in specialist centres
  • Chemotherapy e.g. methotrexate
  • Hysterectomy for PSTT

Risk of metastasis and chemotherapy side effects

41
Q

What do these terms mean and what is the most commonly presented?

  • Lie?
  • Presentation?
  • Attitude?
  • Engagement?
  • Denominator?
  • Position?
  • Station?
  • Caput?
  • Moulding?
A

Lie - longitudinal (99%) or transverse/oblique - position of baby’s spine in relation to mothers

Presentation - what is the presenting part e.g. cephalic, most commonly, or breech (varying types)

Attitude - position of the head which may be well flexed (9.5cm - best for delivery), deflexed, extended or face/hyperextended

Engagement - how many 5ths the head is palpable; if 2/5ths or less palpable then head is engaged, if 3/5ths or more then head is not engaged

Denominator - what foetal part is presenting i.e. most commonly occiput, but may be sacrum, frontal or mentum (chin)

Position - occiput anterior vs left occiput transverse

Station - similar to engagement but determined by vaginal exam; how many cm above or below the ischial spines the baby head is, ranging from -3 to 3 (3cm above IS –> 3cm below IS)

Caput - swelling of the head due to trauma during delivery, can be normal (cephalohaematoma, caput succedaneum)

Moulding - normal during delivery, where normally foetal heads have fontanelle between the parietal bones to enable easier delivery. However, these bones may border each other (+1), cross each other but reducible (+2) or irreducible swelling *****CHECK

42
Q

What is the most common cause for delayed labour?

A

Inefficient uterine contractions

Reasons depend on:

  • Power (^)
  • Passenger (i.e. position of foetus, size)
  • Passage (e.g. smaller pelvis)
43
Q

How many pregnancies are breech at 28w vs at term? What are some risk factors for it?

A

Breech is the opposite of cephalic presentation, where the sacrum/bottom is face down

  • > 25% breech at 28w
  • > 3-5% breech at term

RFs:

  • Maternal = placental abnormalities e.g. PP, uterine abnormalities (shape, fibroids), grand multiparty, polyhydramnios, PREMATURE, small foetus, previous breech, nulliparity
  • Foetal = PREMATURITY, polyhydramnios and oligohydramnios, foetal malformations and congenital abnormalities, SGA and macrosomia
44
Q

How would you identify and confirm breech presentation? What are the 3 types of breech?

A

Ix:

  • > Abdomen examination and find palpable head at the fundus and soft presenting part
  • > Confirmed with USS

Types:

  • Extended/frank breech where sacrum is down but feet up
  • Complete/flexed breech where the sacrum and feet are presenting
  • Footling breech where feet are presenting first
45
Q

How would you manage breech presentation? What are CI’s to CS?

A

Mx:

  • Antenatally:
  • -> Features suggestive of vaginal breech birth being HIGH risk = hyperextended neck, footling presentation, antenatal foetal compromise, low/high EFW
  • Term information
    –> Offer ECV - 50-60% success rate and risk of foetal distress and requiring an emergency CS or going into labour
    CI for ECV include previously planned/required CS, PAH within last 7 days, ROM, multiple pregnancy and amor uterine anomaly
    –> If ECV is unsuccessful or declined then counsel risks of vaginal vs CS birth:
    [CS] = small reduction in perinatal mortality but small risk of immediate complications to mother future pregnancy issues (PP, VBAc, uterine rupture)
    [VB] = lowest risk of complications if successful BUT 40% risk of emergency CS
    –> However, women near the active 2nd stage of labour shouldn’t be offered CS
    –> IOL not recommended and avoided if possible
    –> Continous CTG monitoring
  • -> Vaginal breech delivery:
  • Hands off approach (see notebook for more details)
  • Use of Pinard’s -> Lovesett’s –> Mariceau-Smellie-Veit manouveres
  • Use forceps if required
  • G&S, X-match, FBC, CTG and ensure theatre is ready in case
46
Q

How would you counsel a woman with breech presentation?

A

PACES:

  1. Explain what breech is and RFs present
    - If not at term, explain most babies move to cephalic presentation by term
  2. Explain management - ECV (50% success rate) and CS vs VB and risks/benefits of each i.e. vaginal has lowest risk if successful but 40% risk of needing EMCS vs CS which has small reduction of perinatal mortality but future implications on pregnancies
47
Q

How may a woman with unstable lie present? How can you confirm?

A

Sx:

  • Transverse lie
  • -> Fundal height may be low, no presenting part in pelvis
  • -> Facial landmarks or supraorbital ridges may be felt in Face or Brow presentation

Confirmed with USS

48
Q

How would you manage a woman with unstable lie? What % return to longitudinal lie before labour?

A

Mx:

  • > 80% revert to a longitudinal lie before labour
  • > Impossible to deliver unless cephalic or breech - if in labour with unstable lie then they require immediate CS
  • > Transverse lie = CS (ECV with 50% success, increased risk of cord prolapses)
  • > Brow = CS
  • > Face = mentoposterior requires CS, mentoanterior can be delivered by VD
  • Compound (arm alongside head) = expectantly managed
49
Q

What is oligohydramnios and how common is it? What are some RFs for it?

A

Decreased volume of amniotic fluid/liquor (<5th centile, deepest pool <2cm)
-> Affects 4% pregnancies

RFs:

  • Reduced input fluid –> placental insufficiency, pre-eclampsia
  • Reduced output fluid –> structural pathology (PKD), medications (ACEi, NSAIDs)
  • Lost fluid –> ROM, IUGR, post-term pregnancy carry, TTTS
  • Chromosomal abnormalities
50
Q

How may women with oligohydramnios present?

A

Sx:

  • > PV fluid leakage, ROM
  • > Abdominal exam shows decreased fundal height, foetal parts easily palpable
  • > Speculum may show ROM
51
Q

How would you Ix and Mx women with oligohydramnios? What are complications of it?

A

Ix:

  • > USS for liquor volume and foetal abnormalities
  • > CTG to check foetal wellbeing

Mx:

  • > Term delivery is appropriate, IOL if no CI
  • > Preterm - monitor serial USS for growth, liquor volume, dopplers, regular CTGs, delivery if further abnormalities arise

Complications

  • Labour: emergency CS, meconium liquor, CTG abnormalities
  • Foetal: pulmonary hypoplasia, limb deformities
  • Increased perinatal mortality rates with early onset oligohydramnios
52
Q

What is polyhydramnios defined as? How common is it and what are some RFs for it?

A

Increased amniotic fluid liqour >95th centile, deepest pool >8cm
–> Affects 1-4%

RFs:

  • Failure of foetal swallowing -> neurological/GIT conditions –> chromosomal abnormalities, duodenal or oesophageal atresia
  • Congenital infections
  • Foetal polyuria -> maternal diabetes, TTTS
53
Q

How may women with polyhydramnios present? How would you Ix them?

A

Sx:

  • > Sx of underlying cause e.g. DM
  • > Abdomen - increased fundal height, impalpable foetal parts and tense abdomen

Ix:

  • > USS and liquor volume measurement
  • > Foetal growth, umbilical artery dopplers, CTG, exclude foetal abnormalities
  • > Exclude maternal diabetes
54
Q

How would you manage polyhydramnios and what are the complications of it?

A

Mx:

  • Antenatal monitoring of foetus, ensure DM control and paediatrician present for delivery
  • Amnioreduction (discomfort with gross polyhydramnios)
  • COX inhibitors to reduce foetal urine output

Complications:

  • PTL
  • Malpresentation
  • Placental abruption
  • Cord prolapse
  • PPH
  • Increased risk of CS

Prognosis: increased perinatal morbidity and mortality related to PTL and congenital risks

55
Q

What is Rhesus disease? Who does it affect and what is the process of development?

A

Development of rhesus antibodies in a RhD -ve mother after exposure to RhD +ve blood cells
-> 85% population is Rh+ve, 15% are Rh -ve (these are the patents to worry about)

[RFs = previous pregnancy with insufficient anti-D prophylaxis and previous blood transfusion, although rare in UK]

Process:

  1. Rh- mother has a Rh+ child
  2. Sensitising event mixes blood (note: simple SVD is not a sensitising event)
  3. Mother develops IgM anti-Rh antibodies however, IgM cannot cross the placenta and so doesn’t affect 1st baby
  4. Mother delivers/miscarries child - time passes and mother develops IgG anti-Rh antibodies
  5. Mother has a 2nd Rh+ child and mothers IgG anti-Rh crosses the placenta and can cause progressive fetal anaemia and hydrops fetalis (foetal HF associated with fluid accumulation) if the child is Rh+*
    - > Can do cffDNA to test childs Rh status

*If child is Rh- then no problem, but we assume they are just in case

56
Q

What are sensitising events which can dispose patients to Rh disease?

A

Potentially sensitising events:

  • Amniocentesis, CVS
  • ECV
  • APH/PV bleed (>12w or prolonged if <12w)
  • Ectopic pregnancy
  • Therapeutic or spontaneous (12w+) miscarriage
  • Intrauterine death and stillbirth/molar pregnancy/TOP
  • Abdominal trauma in T3 (26-37w)
  • Intra-operative cell salvage
  • Delivery - if baby is found to be Rh+ at birth then all mothers to receive 500 IU <72h
57
Q

What Ix and Mx is required for suspected/potential Rhesus disease?

A

Ix:

  • Kleihauer test (if 20w+ and determines need for more anti-D)
  • CffDNA testing (12w+)
  • Fathers status
  • Mothers anti-RhD levels

Mx: [only Rh- mothers]

  • Routine antenatal anti-D prophylaxis:
  • -> Indirect antiglobulin testing at booking to check if Abs in serum
  • -> Either 2 doses of 500IU at 28 and 34w OR 1 dose of 1500IU at 28w

+++ Foetal cord bloods post-delivery and prophylaxis in 72h (500 IU anti-D) if baby +ve with Kleihauer test

  • Prophylaxis after sensitising events within 72h of event
  • If mother found to be Rh- and has anti-Rh antibodies at booking then:
  • > monitor titres and if peak above a certain level, monitor baby using MCA dopplers weekly and if the baby is affected, consider IU transfusion
58
Q

When do foetal movements first appear? Why is a reduction in them significant? What questions should you ask these patients and how may you manage these patients?

A
  • -> Foetal movements first appear around 18-20w gestation and ‘rapidly acquire a regular pattern’ [RCOG]. Note: Primips tend to be 20w+ and Multips may feel them from 16w
  • -> Red flag = none by 24w
  • -> Movements tend to increase until ~32w, then tend to plateau but NO reduction in the frequency until labour
  • -> A reduction in movements can be seen as a warning sign for impending foetal death/compromise (stillbirth)

Qs to ask in RFM Hx:

  • > How long have you noticed this?
  • > What made you notice this - was it a change in frequency or strength or both?
  • > Have you experienced reduced movements before - if so, probe further?
  • > Any conditions/issues during antenatal period so far, any previous complications in pregnancies etc? Previous stillbirths and FGR and RFs for stillbirth - i.e. pre-eclampsia+HTN, DM, extreme maternal ages, primips etc)

Ix + Mx:

  • > If concerned about movements they should contact maternity unit
  • > Pregnant abdomen exam + Doppler for foetal HR and check baby is alive
  • > At least 20min CTG for foetal monitoring and assess compromise BUT only if 28w+ (however is just a ‘snapshot’)
  • > Consider USS if CTG normal but maternal perception of movements is still reduced OR additional RF’s for stillbirth/FGR –> check AC/EFW to check if restricted growth and fluid volume, and foetal morphology if not done so already and mother agrees
  • > Reassure if normal = 70% of those who present with one episode reduced foetal movements have a normal outcome to pregnancy - but if feel reduced again, they should come back and be monitored again at the maternity assessment unit
59
Q

What is the difference between N+V in pregnancy and hyperemesis gravidarum? What is the difference in their prevalence and how do they present?

A

Both HG and N+V in pregnancy occur within the 1st trimester:

  • N+V is very common, affecting ~80-90% women (emesis gravidarum)
  • N+V peaks around 8-12w, starting around 4-7w and ending 16-20w
  • HG affects 1% of women

Sx:

  • HG Dx requires the triad of:
  • –> Dehydration
  • –> 5%/+ pre-pregnancy weight loss
  • –> Electrolyte imbalance
  • Vomiting and inability to tolerate both fluids and food
  • Starts between 4th-7th week, peaking at 9th week
  • Resolves by 20w
  • Exclude other causes e.g. H.pylori, infection, drugs, abdominal pain
60
Q

What are some RFs for hyperemesis gravidarum, and what is the aetiology?

A

HG is the extreme form of N+V in pregnancy, and both are caused by the rise in bHCG levels in pregnancy
-> The higher the bHCG levels, the greater the Sx

RFs:

  • Multiple pregnancy
  • Molar pregnancy and trophoblastic disease
  • Previous HG
  • Nulliparity (1st pregnancy)
  • Hyperthryoid
  • Obesity

Smoking is protective!

61
Q

How would you Ix a woman presenting with suspected hyperemesis gravidarum? What score can be used to assess severity?

A

Ix:

  • Examination for signs of dehydration and abdominal pain
  • Obs - HR, RR, Sats, BP
  • Weight measurement
  • Urine dipstick for ketones
  • Bloods - U&Es, FBC

PUQE-24 score

  • > If severe, i.e. 13/+ score then admit patient
  • > From RCOG guidelines
  • > Asks how many times in last 24h, pt has i) felt nauseated/sick to stomach ii) vomited iii) retched without bringing anything up as well as sleep quality and affect on QoL
62
Q

How would you manage hyperemesis gravidarum?

A

Mx:

  • > Admission if unable to keep down fluids/oral antiemetics, ketonuria, weight loss and co-morbidities e.g. DM (+severe as per PUQE score)
  • > Admitted pt = IV normal saline with KCl and thiamine supplementation
  • > If mild/moderate/not severe, then treat in day case/ambulatory care
  • > 1st line = antihistamines such as IV prochlorperazine (Stemetil) OR cyclizine
  • > 2nd line = antiemetics such as IV ondansetron or metaclopramide + reassess in 24h [2nd line as risks of EPSE with metaclopramide and ondasetron has unknown effects in pregnancy]
  • > 3rd line = steroids (IV hydrocortisone BD 100mg, converting to PO when able)

note:

  • Combinations may be used if single drug is ineffective
  • If admitted, remember VTE prophylaxis !! (LMWH)
63
Q

What are the complications of hyperemesis gravdiarum? How would you counsel patients with it?

A

Complications:

  • Maternal = VTE, MW tear, Wernicke’s encephalopathy from low B1, dehydration and hyponatremia/hypokalaemia
  • Foetal = IUGR, PTL, Termination

PACES:

  • > Explain results and diagnosis - extreme form of N+V in pregnancy, RFs involved e.g. multiple/1st pregnancy
  • > Explain plan - fluids + electrolytes/minerals as can’t tolerate oral and some medications to reduce nausea such as prochlorperazine
  • > Usually peaks around 8-12w/ and then gets better after 12-14w and go away by 16-20w
  • > Safety netting - if it gets worse, can’t tolerate fluids still and not improving then come back
  • > Stress important of adequate fluid intake and nutrition
64
Q

Why are pregnant women at increased risk of UTI and bacteriuria in pregnancy? How is this managed and why?

A

Many causes:

  • > Increased glycosuria in pregnancy which therefore is more attractive to bacteria
  • > Compression of bladder by uterus + ureteric dilation
  • > Immunocompromised in pregnancy

Pregnant women have their urine MC+S and dipsticks done regularly at appointments + at booking to check for asymptomatic bacteriuria
Risks of UTI to pregnancy = preterm delivery, LBW and PET

65
Q

How may women present with a UTI in pregnancy?

A

Sx:
FUND HIPS
-> Frequency, urgency, nocturia, painful or burning sensation when urinating, blood or mucus in urine
-> Lower abdomen/loin pain
-> Foul smelling urine
-> Dyspareunia
-> Fever, rigors, lower abdomen pain (pyelonephritis)

66
Q

How would you investigate suspected UTI in pregnant women?

A

Ix:

  • > Obs (fever, HR, RR etc)
  • > Urinalysis (nitrites and leukocytes, nitrites more accurate indication of of UTI)
  • > Urine MC+S
67
Q

How would you manage suspected UTI in pregnant women? What must be avoided and why?

A

Mx:

  1. Asymptomatic bacteruria as seen via MC+S
    - Immediate Abx treatment for 7d of either Nitrofurantoin* 100mg BD OR Amoxicillin*** 500mg TDS OR Cephalexin 500mg TDS
    - If GBS identified then write in notes as will require intrapartum IV BenPen
  2. UTI in pregnancy [no visible haematuria]
    - MSU before Abx start
    - Analgesia, avoid dehydration
    - Immediate Abx treatment for 7d of Nitrofurantoin 100mg BD [2nd line = Amoxicillin or Cephalexin 100mg TDS)
  3. Pyelonephritis
    - Cephalexin or Cefuroxime
    - Risk of LBW and pre-term delivery
  • Nitrofurantoin can be given in pregnancy BUT AVOIDED in the third trimester/at term due to risk of neonatal haemolysis
  • *Trimethoprim is contraindicated in the first trimester due to its action as a folate antagonist and so increases risks of NTDs
  • **Amoxicillin only after sensitivities known
68
Q

What organisms may cause UTI in pregnancy?

A

Same as non-pregnant individuals - E. coli, Klebsiella, Enterococcus, Pseudomonas, Candida

69
Q

What are the 4 categories of C sections? What are the 2 traditional incisions used?

A

Category 1: Immediate threat to life to mother or baby, decision to delivery = 30 mins

Category 2: Not an imminent threat to life but CS required urgently to avoid compromise to mother or baby, decision to delivery = 75 mins

Category 3 = CS delivery required but mother and baby are stable

Category 4 = elective [pre-planned]

Incisions:
Pfannenstiel - lower, curved incision, 2 finger width above the pubic symphysis

Joel-Cohen = straight incision, slightly higher (recommended)

Midline scar is rare, sometime used for very premature babies or anterior placenta praaevia

70
Q

What are some reasons for an elective CS? Why is spinal anaesthetic preferred to GA and what are their side effects?

A
  • Previous CS
  • Placenta praevia, vasa praevia
  • Multiple pregnancy
  • Breech (especially footling)
  • Uncontrolled HIV
  • Previous perineal injury which is symptomatic
  • Cervical cancer

Spinal e.g. lidocaine, is safer and leads to fewer complications + patient is awake

  • SE’s of spinal = hypotension, haematoma at site of injection, urinary retention (place catheter), anaphylaxis etc
  • GA can impact baby - floppy, sedated neonate BUT may be used if immediate/rapid induction of anaesthesia required
71
Q

What measures are taken during a CS to reduce risk? [4]

A

Risk prevention:

  • H2 recetor antagonist/PPIs before the procedure (aspiration pneumonia)
  • Abx prophylaxis
  • VTE prophylaxis with LMWH
  • Oxytocin to reduce PPH risk
72
Q

What are some 2 forms of monitoring during labour?

A

1 - Intermittent auscultation of foetal HR for at least 60s immediately after a contraction

  • -> 1st stage = at least every 15 mins
  • -> 2nd stage = at least every 5 mins or after every contraction

2 - Continuous cardiotocography (electronic foetal monitoring)

  • -> Indicated if antenatal or intrapartum RFs
  • -> Results in increased intervention, no marked reduction in CP
73
Q

What are some indications for CTG monitoring?

A

Antenatal:

Maternal = previous CS, cardiac problems, DM, PROM >24h, IOL, APH, PET, other significant maternal medical conditions

Foetal = IUGR, prematurity, oligohydramnios, multiple pregnancy, meconium stained liquor, breech, abnormal dopplers

Intrapartum = maternal pulse >120bpm, maternal temperature >38 single reading or 2 consecutive >37.5, suspected sepsis/chorioamnionitis, significant meconium, delay in labour, oxytocin use, abnormal FHR on intermittent auscultation

74
Q

Outline the systematic approach to reading a CTG?

A

DR C BRaVADO

DR - define risk i.e. maternal background, intrapartum and obstetric complications e.g. maternal sepsis/PROM/IUGR

C - contractions

BRa - baseline rate of foetus (normally 110-160)

V - variability

A - accelerations

D - decelerations

O - overall impression

75
Q

How would you comment on the contractions?

A

At the bottom of the CTG, is the uterine contractions
You could comment on the:
- Frequency (number of contractions in 10 mins - each big square = 1 minute )
- Duration, regularity
- NOTE: intensity of contractions can only be assessed with palpation of contraction (NOT on CTG itself)

76
Q

How would you assess the BRa? What is classed as non-reassuring or abnormal and what are some causes for this?

A

Foetal baseline rate:

  • > Avg HR of the foetus within a 10 minute window
  • > IGNORE any accelerations or decelerations
  • > Normal HR = 110-160
  • > Non reassuring = 100-109 and 161-180

> 160 for 3 mins/+ = foetal tachycardia

  • -> Causes include foetal hypoxia, chorioamnionitis, hyperthyroidism, fetal or maternal anaemia and fetal tachyarrythymia
  • -> Above 160 is NR, >180 is abnormal

<110bpm for 3 mins/+ = foetal bradycardia

  • -> Causes include post-dates gestation, prolonged cord compression, cord prolapse, epidural and spinal anaesthesia, rapid foetal descent and maternal seizures
  • -> If the cause can’t be identified and corrected then immediate delivery recommended
77
Q

What is variability and what might it be due to?

A

Variability describes the variation of foetal HR from one beat to the next (look at how the peaks and troughs vary from the baseline rate)

Normal variability = 5-25bpm

Non-reassuring = <5pm for between 30-50 mins
OR
>25bpm for 15-25 mins

Abnormal = <5pm but >50 mins
OR
>25 bpm for >25 mins

CAUSES:
Most common reason for reduced variability is due to fetal sleeping (usually ~40 mins max) = PHYSIOLOGICAL

Other causes = fetal acidosis due to hypoxia, fetal tachycardia, drugs (BZD/opiates/MgSO4/methyldopa), prematurity (<28w) and congenital heart abnormalities

78
Q

What are accelerations and what do they signify?

A

Accelerations = abrupt increases in baseline FHR >15pm for 15/+ seconds

You should just comment on their presence

  • > If present, it is reassuring
  • > Sign of a healthy foetus when occurring alongside uterine contractions
  • > Absence of accelerations in an otherwise normal CTG is of uncertain significance
79
Q

What are decelerations? What are the 4 different types and what do they signify?

A

Abrupt decrease in baseline FHR >15bpm for >15 seconds
-> Due to response to hypoxic stress, the foetus reduces its HR to preserve myocardial oxygenation and perfusion

They may be:
Early, Variable, Late or prolonged

  1. Early decelerations
    - Physiological
    - Occur in late 1st stage and 2nd stage of labour
    - Occur with the onset of a uterine contraction and RESOLVES when the contraction stops
    - Due to head compression (raised ICP) and subsequent stimulation of the PNS via vagus nerve
  2. Variable decelerations
    - Occur at a variable relationship to contractions
    - Usually due to cord compression
    - ‘Shouldering’ (= peak either side of deceleration, indicates cord compression)
    - Concerning features include VDs that are = >60s, no ‘shouldering’, reduced baseline variability within the decoration, failure to return to baseline and biphasic ‘W’ shape
    - No shouldering suggests fetus is becoming hypoxic
    - Variable decelerations with no concerning characteristics for <90 mins is classed as reassuring
  3. Late decelerations
    - Pathological
    - Begin at the peak of a uterine contraction and recover AFTER the contraction ends
    - Causes include maternal hypotension, PET and uterine hyper stimulation (e.g. too much oxytocin)
    - Concerning for foetal hypoxia
    - Management with conservative measures (LL position, foetal blood sampling and expedite delivery)
  4. Prolonged decelerations
    - Deceleration >3 mins which is abnormal [2-3 mins is non-reassuring)
    - Action must be taken quickly i.e. foetal blood sampling or EMCS
80
Q

What is a sinusoidal pattern indicative of on a CTG?

A

Sinusoidal CTG:

  • Very rare
  • Concerning
  • Smooth regular wave-like pattern with no beat-to-beat variability
  • Usually requires immediate CS
  • Indicates at least 1/+ of severe fatal hypoxia, severe fatal anaemia or fatal/maternal haemorrhage
81
Q

How would you comment on the overall impression of a CTG? What is your management depending on this?

A

Overall impression:

  • -> Normal = all features are reassuring
  • -> Suspicious = 1 non-reassuring feature but rest reassuring
  • -> Pathological = 1 abnormal feature or 2 non-reassuring features

Mx:
Normal = continue CTG and inform mother + companion of whats happening

Suspicious =

  • -> Conservative - place in left lateral position to avoid IVC compression and increase venous return
  • -> Correct any underlying cause e.g. fluids if hypotensive or stop/reduce synto if uterine hyper stimulation
  • -> Inform senior midwife or obstetrician
  • -> Document plan and inform mother + companion

Pathological =

  • -> Review by senior midwife AND obstetrician
  • -> Exclude any acute causes e.g. cord prolapse, abruption or uterine rupture
  • -> Conservative - place in left lateral position to avoid IVC compression and increase venous return
  • -> Correct any underlying cause e.g. fluids if hypotensive or stop/reduce synto if uterine hyper stimulation
  • -> Review by senior midwife AND obstetrician
  • -> IF still pathological after conservative measures then offer digital scalp stimulation and document outcome (should increase FHR)
  • -> IF still pathological then consider foetal blood sampling + expedite delivery by either CS or instrumental (taking mothers preferences into account)
  • -> Document plan and inform mother + companion
82
Q

What are some physiological changes that occur in pregnancy? Think:

  • Weight (& foetal weights)
  • Cardiac
  • Haematological
  • Respiratory
  • GI
  • Renal
  • Endocrine
A

Most women put on 10-12.5kg during their pregnancy which can be due to

  • Body fat
  • Baby*, placenta, amniotic fluid
  • Fluid retention
  • Increased blood volume
  • Breast enlargement

Note: foetal weight gain is 100g/week before 28w, then 200g/week after 28w
- Baby usually 2.5-4.5kg at term, placenta ~600g at term

Cardiac:

  • > PVR decreases by nearly 50% due to vasodilator prostaglandins
  • > Decrease in BP by mid-pregnancy by 10-20mmHg, later increasing to non-pregnant levels by term
  • > SV increases by 35% and Hr increase by 15-25%
  • > Therefore, increased CO (by 40% in T3)
  • –> In labour, CO = 9L per min, with 1L/min going to the uterus
  • > Changes to prepartum state 2w after delivery

Respiratory:

  • > Significant increase in O2 demand
  • > Tidal volume increased 30-50% (-> increase in Minute Ventilation which = TV x RR) - progesterone effect
  • > RR doesn’t change! Hyperventilation to supply demand may occur/subjective breathlessness

Haematology:

  • > Macrocytosis (20% in size) + dilutational anaemia (lower HCT)
  • > Neutrophilia
  • > Plts decrease but still within normal limits
  • > Most clotting factors increase (F8, 9 and 10) + fibrinogen levels but PT and APTT are unchanged
  • > Increased plasma volume by 30-50%
  • > Varicose veins common due to venous stasis and venodilation

GI:

  • N+V
  • Decreased oesophageal sphincter tone (reflux)
  • Reduction in GIT motility by progesterone on smooth muscle relaxation, which may cause constipation

Endocrine:

  • > Hypocalcaemia and Vit D deficiency are common in pregnancy
  • > Prolactin increases 10-fold
  • > Biggest increase is in oestriol, with lesser increases in oestrogen and estradiol
  • > LH and FSH suppressed

Renal:

  • > Increased proteinuria and glycosuria (+oedema)
  • > GFR increases
  • > Increased RAAS activation leading to increased fluid retention and blood volume
  • > Hydronephrosis is common and physiological due to right ureter crossing iliac and ovarian vessels at an angle before entering pelvis
  • > Diuresis for 7d postnatally
83
Q

What are some RFs for a high-risk pregnancy?

A

Medical:

  • > Previous high-risk pregnancy/complications !!
  • > <15yo or >35yo
  • > Hyper/Hypothyroid
  • > Under 5ft, small pelvis, PPW <45kg or obese

Socioeconomic:

  • > Single mother
  • > Low SE status
  • > No access to early prenatal care
  • > Illicit drug use
  • > Smoker or Alcohol use
84
Q

Why is obesity in pregnancy important?

A

Obesity = BMI >30

  • > Increases the risk antenatally e.g. PET, GDM, infections
  • > Increases risks of intrapartum complications e.g. may require CS/IOL
  • > Advise conservative measures and post-natal T2DM f/u
85
Q

What cardiac signs are normal in pregnancy?

A
  • ESM in 96% - increased CO
  • 3rd heart sound in 84% - increased volume
  • Forceful apex beat
  • Peripheral oedema
86
Q

What form of multiple pregnancy has the best outcome?

A

Dichorionic diamniotic twins

  • > Separate placentas and nutrient supply
  • > Separate amniotic sacs
87
Q

When is multiple pregnancy normally detected? What signs help distinguish this?

A

Normally detected at dating USS scan (10-14w). Also find:

  • > Gestational age
  • > Chorionicity and amnionicity (number of each)
  • > Risk of Down’s (as part of combined test - along with PAPP-A and free b-HCG)

USS signs:

  • > Lambda sign/Twin peak sign = dichorionic diamniotic twins (where membrane meets chorion between twins)
  • > T sign = monochorionic diamniotic
  • > Monochorionic monoamniotic twins have no membrane separating them
88
Q

What are the risks associated with multiple pregnancy?

A

Risk to mother

  • Polyhydramnios
  • Anaemia
  • Malpresentation
  • Spontaneous preterm birth
  • CS
  • PPH
  • HTN
  • Hyperemesis gravidarum

Risks to foetuses and neonates:

  • Miscarriage and stillbirth
  • FGR
  • Prematurity
  • TTTS
89
Q

What is twin-twin transfusion syndrome and its results? How may it be treated?

A

When the twin foetuses share a placenta and there is a connection between both their blood supply

  • -> One twin (recipient) receives a majority of the placental blood whereas the other (donor) is starved of food
  • -> There recipient may become fluid overloaded, with HF and polyhydramnios
  • -> The donor may have FGR, anaemia and oligohydramnios

Women with TTTS need to e referred to a tertiary specialist foetal medicine centre
- In severe cases, laser treatment may be used to destroy the connection between the 2 blood supplies

90
Q

What is twin anaemia-polycythaemia sequence?

A

Another complication of multiple pregnancy, similar to TTTS but less acute
-> One twin becomes anaemic whilst the other develops polycythaemia

91
Q

Describe the management of multiple pregnancy? (Ante vs Intra vs PP)

A

Antenatal care:

  • > Dr-led: Special multiple pregnancy obstetric team management
  • > Additional monitoring for anaemia at 20w, in addition to routine booking +28w FBC
  • > Additional USS + Dopplers to monitor for FGR, unequal growth and TTTS = every 2w from 16w if monochorionic OR every 4w from 20w if dichorionic
  • > Corticosteroids for lung maturation e..g if MM early delivery

Intrapartum:
-> Elective CS offered at either:
–> 32(-33+6)w for uncomplicated monochorionic monoamniotic twins
–> 36(-+6)w for uncomplicated monochorionic diamniotic twins
–> 37(-+6)w for uncomplicated dichorionic diamniotic twins
–> ~35w for triplets
NOTE: Vaginal birth is possible in diamniotic twins, when first baby is cephalic - CS may be required for 2nd baby (4% risk)

Ensure to inform that continuing an uncomplicated pregnancy beyond these points is associated with an increased risk of FOETAL DEATH
–> Also explain risk of PRE-TERM birth (60% twins before 37w and 75% triplets born before 35w) hence why choose these dates

If elective birth is declined, offer weekly appointments with specialist obstetrician (including weekly Doppler US and fortnightly growth scans)