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Phase 3a > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

Describe the features of an obstetric history

A
  • 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
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2
Q

What are the common symptoms in an obstetric history?

A
  • 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)
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3
Q

What is gestational age?

A
  • 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
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4
Q

What are the stages of labour

A
  • 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
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5
Q

Define gravidity and parity

A
  • 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)
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6
Q

Define nulliparous, primiparous, and multiparous

A
  • Nulliparous: never delivered a baby
  • Primiparous: delivered one baby (often used interchangeably with primigravida but not technically correct)
  • Multiparous: delivered more than one baby
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7
Q

Describe the first stage of labour

A
  • 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)
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8
Q

Describe the second stage of labour

A
  • 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)
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9
Q

How long is each stage of labour?

A
  • 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
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10
Q

Describe the cardinal movements of labour?

A
  • 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
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11
Q

What are Braxton-Hicks contractions?

A
  • Occasional irregular contractions of the uterus
  • Felt during the second and third trimester
  • Do not indicate the onset of labour, known as ‘practice’ contractions
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12
Q

Describe the foetal lie, presentation, and position

A
  • 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)
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13
Q

Define pre-eclampsia

A

New onset of hypertension (over 140 systolic or 90 diastolic) a 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)

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14
Q

Define eclampsia

A

The occurrence of one or more seizures in woman with pre-eclampsia, which is an obstetric emergency

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15
Q

Define HELLP syndrome

A

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

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16
Q

What causes pre-eclampsia?

A

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

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17
Q

What are the risk factors for pre-eclampsia?

A

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

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18
Q

When is prophylaxis for pre-eclampsia indicated?

A
  • Women with 1 high risk factor or 2 or more moderate risk factors
  • Aspirin 75mg a day, from 12 weeks gestation until birth
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19
Q

What are the symptoms of pre-eclampsia?

A
  • 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
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20
Q

What anti-hypertensives are used in pregnancy, and what are their side effects?

A
  • 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
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21
Q

What is the management of pre-eclampsia?

A
  • 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
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22
Q

What is the inpatient management of severe pre-eclampsia?

A
  • 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
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23
Q

What is the management of eclampsia?

A
  • 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
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24
Q

What causes antepartum haemorrhage?

A
  • 40% are unidentifiable cause
  • Low lying placenta/placenta praevia
  • Vasa praevia
  • Minor/major abruption
  • Infection
  • Trauma/domestic violence
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25
Q

What are the management of antepartum haemorrhage?

A
  • 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
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26
Q

Define placenta praevia

A

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)

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27
Q

What are the risk factors for placenta praevia?

A
  • 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
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28
Q

What are the clinical features of placenta praevia?

A
  • 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
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29
Q

What is the management of placenta praevia?

A
  • 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
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30
Q

Describe vasa praevia

A
  • 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
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31
Q

Describe morbidly adherent placenta

A
  • 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
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32
Q

Describe placental abruption

A
  • 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
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33
Q

What are the complications of antepartum haemorrhage?

A
  • Premature labour/delivery
  • Need for bloodtransfusion
  • Acute tubular necrosis (+/- renal failure)
  • DIC
  • PPH
  • ITUadmission
  • ARDS (secondary to transfusion)
  • Foetalmorbidity (hypoxia) andmortality
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34
Q

What are the risk factors for maternal sepsis?

A
  • 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
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35
Q

What is the management of maternal sepsis?

A

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

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36
Q

Describe cord prolapse

A
  • 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
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37
Q

What are the risk factors for cord prolapse?

A
  • 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
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38
Q

What is the management of a cord prolapse?

A
  • 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
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39
Q

Define shoulder dystocia

A

Failure for the anterior shoulderto pass under the symphysis pubisafter delivery of thefoetalhead

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40
Q

What are the risk factors for shoulder dystocia?

A
  • 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
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41
Q

What is the management of shoulder dystocia?

A

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

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42
Q

What are the complications of shoulder dystocia?

A

Maternal:
- PPH
- extensive vaginal tear
- psychological
Foetal:
- hypoxia (seizures, cerebral palsy)
- injury to brachial plexus
- humeral fracture

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43
Q

Define post partum haemorrhage

A
  • Primary: within 24 hours
  • Secondary: after 24 hours up to 12 weeks
  • Minor: 500-1000 mls
  • Major: >1000 mls
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44
Q

What are the causes of primary post partum haemorrhage?

A

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)

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45
Q

What are the risk factors for post partum haemorrhage?

A
  • Big baby
  • Nulliparity andgrandmultiparity
  • Multiple pregnancy
  • Precipitate orprolonged labour
  • Maternal pyrexia
  • Operative delivery
  • Shoulder dystocia
  • Previous PPH
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46
Q

What is the management of primary post partum haemorrhage?

A

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

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47
Q

What are the causes of post-partum haemorrhage?

A
  • 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

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48
Q

What is the management of secondary post partum haemorrhage?

A
  • Resuscitation if needed
  • IV antibiotics if infectious cause
  • Uterotonics (sytocinon, ergometrine, misoprostol)
  • Surgical measures
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49
Q

What does a portogram record?

A
  • Progress of labour
  • Foetal condition
  • Maternal condition
  • Space for drugs, IV, etc.
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50
Q

What does station refer to during labour?

A

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)

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51
Q

Describe the anatomy of the foetal skull

A
  • 4 bones: occipital, temporal, parietal, frontal
  • Anterior fontanel: frontal suture, coronal suture, sagittal suture (diamond shaped)
  • Posterior fontanel: sagittal suture, lambdoid suture (triangle shape)
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52
Q

What are the diameters of the foetal skull?

A
  • Suboccipital bregmatic: well flexed, 9.5cm
  • Occipital frontal: deflexed, 10.5cm
  • Mento vertical: extended (brow), 13cm
  • Submental bregmatic: hyperextended, 9.5cm
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53
Q

Describe the pain pathway in labour

A

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

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54
Q

What are the non-pharmacological managements in labour?

A

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

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55
Q

What are the medical forms of pain relief used in labour?

A

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

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56
Q

What are the different categories for C section?

A
  • 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)
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57
Q

What hormones are important in labour?

A
  • 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
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58
Q

Describe the pelvic inlet and outlet

A

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

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59
Q

Describe the rupture of membranes

A
  • Can be spontaneous (SROM) or artificial (ARM)
  • SROM can happen at any point prior to, or during labour
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60
Q

What is the function of amniotic fluid and sac?

A

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)

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61
Q

What blood vessels are in the umbilical cord?

A
  • 1 vein (oxygenated blood and nutrients from placenta to baby)
  • 2 arteries (carry waste away from baby)
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62
Q

What are the indications for induction of labour?

A
  • 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
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63
Q

What are the contraindications of induction of labour?

A

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 of higher pregnancy
- 2 or more previous low transverse C sections

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64
Q

Describe vaginal prostaglandins for induction of labour?

A
  • 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
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65
Q

Describe amniotomy for induction of labour

A
  • 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
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66
Q

Describe membrane sweep for induction of labour

A
  • 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
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67
Q

Describe cervical ripening balloon for induction of labour

A
  • 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
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68
Q

What things determine the ripeness of the cervix (Bishop score)?

A
  • Dilation
  • Length (effacement)
  • Station
  • Consistency
  • Position
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69
Q

What are the complications of induction of labour?

A
  • 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
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70
Q

What are the indications for an instrumental delivery?

A
  • 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
71
Q

Describe a ventouse delivery

A
  • 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
72
Q

Describe a forceps delivery

A
  • 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
73
Q

What are the pre-requisites for instrumental delivery?

A
  • 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
74
Q

What are the contraindications of instrumental delivery?

A

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

75
Q

What are the complications of instrumental delivery?

A

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

76
Q

What are the different types of perineal tear?

A
  • 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
77
Q

What is the management of perineal tears?

A
  • First degree: heal without treatment
  • Second degree: require sutures to repair muscle
  • Third and fourth: require specialist repair in theatre
78
Q

What things dose a CTG monitor?

A
  • Foetal heart rate
  • Contractions of the uterus
79
Q

What are the indications for continuous CTG monitoring in labour?

A
  • Sepsis
  • Maternal tachycardia (>120)
  • Pre-eclampsia (particularly >160/110)
  • Fresh antepartum haemorrhage
  • Delay in labour
  • Disproportionate maternal pain
  • Use of oxytocin
  • Significant meconium
80
Q

What mnemonic is used to assess CTGs?

A

Dr C BRAVADO
- DR: Define Risk
- C: Contraction
- BRa: Baseline Rate
- V: Variability
- A: Acceleration
- D: Deceleration
- O: Overall

81
Q

How are contractions analysed on a CTG?

A
  • 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
82
Q

How is the baseline rate assessed in a CTG?

A
  • 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
83
Q

What are the causes of foetal tachycardia/bradycardia?

A

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

84
Q

How is variability assessed on a CTG?

A
  • 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
85
Q

What are the causes of reduced variability?

A
  • 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
86
Q

Describe accelerations on a CTG

A
  • 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
87
Q

How are decelerations assessed in a CTGs?

A
  • 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
88
Q

Describe early decelerations on a CTG?

A
  • 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
89
Q

Describe late decelerations on a CTG

A
  • 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
90
Q

Describe variable decelerations on a CTG

A
  • 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
91
Q

Describe prolonged decelerations

A
  • 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
92
Q

Describe a sinusoidal pattern in a CTG

A
  • 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
93
Q

What are the different categories of the overall impression of a CTG?

A
  • 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
94
Q

What is the rule of 3s for prolonged foetal bradycardia?

A
  • 3 minutes: call for help
  • 6 minutes: move to theatre
  • 9 minutes: prepare for delivery
  • 12 minutes: deliver the baby
95
Q

What are the risk factors for small for gestational age?

A

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

96
Q

Define intrauterine growth restriction

A
  • 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
97
Q

What are the causes of intrauterine growth restriction?

A
  • Pre-existing maternal disease (e.g. renal, autoimmune)
  • Maternal pregnancy complications (e.g. pre-eclampsia)
  • Multiple pregnancy
  • Smoking and drug use
  • Infection (e.g. CMV)
  • Extreme exercise
  • Malnutrition
  • Congenital or chromosomal abnormalities
98
Q

What is the management of intrauterine growth restriction?

A
  • 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 and umbilical artery dopplers
  • Indication for emergency C-section = absent or reversed end-diastolic flow
99
Q

Define prolonged pregnancy

A
  • More than 42 weeks gestation
  • Common with previous prolonged pregnancies, and nulliparity
  • Increased risk of stillbirth, neonatal illness, meconium passage, foetal distress
100
Q

What is the management of prolonged pregnancies?

A
  • 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
101
Q

Define preterm delivery

A
  • 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
102
Q

What are the risk factors for spontaneous preterm labour?

A
  • 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
103
Q

What are some methods of prevention of preterm labour?

A

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:
- suppositories 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

104
Q

What is the management of spontaneous preterm labour?

A
  • 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 die to higher risk of GBS
105
Q

What are the complications of spontaneous preterm labour?

A

Foetal:
- need for neonatal intensive care
- cerebral palsy
- perinatal mortality
- chronic lung diseases
- cognitive development problems
Maternal:
- infection
- need for C section

106
Q

What are the indications for pre-term delivery?

A

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

107
Q

Define Rhesus haemolytic disease

A
  • 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
108
Q

What are potential sensitising events in pregnancy?

A

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

109
Q

How is Rhesus disease prevented in pregnancy?

A
  • 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
110
Q

What is the Kleihauer test?

A
  • 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
111
Q

Describe the pathophysiology of diabetes in pregnancy

A
  • Pregnancy is a state of physiological insulin resistance and relative glucose intolerance
  • Altered 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
112
Q

What are the risk factors for gestational diabetes?

A
  • 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
113
Q

What are the clinical features and complications of gestational diabetes?

A

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

114
Q

What investigations are needed for gestational diabetes?

A

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

115
Q

What is the diabetes management of gestational diabetes?

A
  • 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)
116
Q

What is the obstetric management of gestational diabetes?

A
  • 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
117
Q

What is the postnatal management of gestational diabetes?

A
  • 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
118
Q

What are the effects of pregnancy on pre-existing diabetes?

A
  • 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)
119
Q

What are the risks and complications of pre-existing diabetes in pregnancy?

A

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

120
Q

What is the diabetes management of pre-existing diabetes in pregnancy?

A
  • 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
121
Q

What is the obstetric management of pre-existing diabetes in pregnancy?

A
  • 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
122
Q

What is the post-natal care of pre-existing diabetes?

A

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

123
Q

Define antepartum haemorrhage

A
  • Bleeding from anywhere within the genital tract after the 24th week of pregnancy
  • Occurs in 3-5% of pregnancies
124
Q

Define obstetric cholestasis

A

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

125
Q

What are the risk factors for obstetric cholestasis?

A
  • Past history (recur more severely in 50%)
  • Family history
  • Multiple pregnancy
  • Presence of gallstones
  • Hepatitis C
126
Q

What is the presentation of obstetric cholestasis

A
  • 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)
127
Q

What are the investigations needed for cholestasis?

A
  • 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
128
Q

What is the management for obstetric cholestasis?

A
  • 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
129
Q

What are the complications of obstetric cholestasis?

A
  • Increased risk of sudden intrauterine death
  • Increased risks during delivery: premature, intrauterine asphyxia, foetal bradycardia,
  • Maternal morbidity due to itching and lack of sleep
130
Q

What are the risk factors for VTE during pregnancy?

A

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

131
Q

How is the risk of pregnancy related VTE managed?

A

Non-pharmacological:
- mobilisation
- hydration
- compression stockings
Low molecular weight heparin:
- antenatal prophylaxis (if high risk)
- postnatal prophylaxis (10 days for lower risk, 6 weeks or higher risk)
- immediate treatment of VTE (stopped before labour)

132
Q

What is the cause of anaemia during pregnancy?

A

Disproportionate increase of plasma volume and red blood cell mass, leading to an overall decrease of haemoglobin concentration due to a haemodilution effect

133
Q

What are the risk factors for anaemia during pregnancy?

A
  • Haemoglobinopathies (thalassaemia, sickle cell disease)
  • Increased maternal age
  • Anaemia during previous pregnancies
  • Poor diet
  • Low socioeconomic status
134
Q

How is anaemia during pregnancy managed?

A
  • 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)
135
Q

Define group B streptococcus infection in pregnancy

A
  • 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
136
Q

What are the risk factors for group B streptococcus infection in neonates?

A
  • 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
137
Q

How is group B streptococcus infection in pregnancy managed?

A
  • 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
138
Q

Define hyperemesis gravidarum

A

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

139
Q

What is the pathophysiology of hyperemesis gravidarum?

A

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

140
Q

What are the risk factors for hyperemesis gravidarum?

A
  • First pregnancy
  • Previous history
  • Raised BMI
  • Multiple pregnancy
  • Hydatidiform mole
141
Q

What are the investigations for hyperemesis gravidarum?

A
  • 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)
142
Q

What is the management for hyperemesis gravidarum?

A
  • 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

143
Q

Define oligohydramnios

A

Low levels of amniotic fluid during pregnancy, defined as being below the 5ht centile for the gestational age

144
Q

What are the causes of oligohydramnios?

A
  • 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)
145
Q

How is oligohydramnios assessed?

A

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)

146
Q

What is the management of oligohydramnios?

A

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

147
Q

What are the complications of oligohydramnios?

A
  • Potter syndrome
  • Pulmonary hypoplasia
  • Foetal compression syndrome
  • Amniotic band syndrome
  • Increased risk of foetal infection
148
Q

Define polyhydramnios

A

Abnormally large levels of amniotic fluid during pregnancy, defined as being above the 95th centile for gestational age

149
Q

What are the causes of polyhydramnios?

A
  • 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
150
Q

How is polyhydramnios assessed?

A

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)

151
Q

What is the management for polyhydramnios?

A
  • 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)
152
Q

What are the complications of polyhydramnios?

A
  • Preterm delivery
  • Placental abruption
  • Malpresentation
  • Postpartum haemorrhage
  • Cord prolapse
153
Q

Define foetal hydrops

A

Abnormal fluid accumulation in two or more foetal compartments (abdominal, pleural, skin)

154
Q

What are the causes of foetal hydrops?

A

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

155
Q

What investigations are needed for foetal hydrops?

A
  • 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
156
Q

What is the management of foetal hydrops?

A

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

157
Q

Describe the different types of prenatal testing for congenital abnormalities

A

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%)

158
Q

Describe cytomegalovirus in pregnancy?

A
  • 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
159
Q

Describe herpes simplex infection in pregnancy

A
  • Background: manifests as cols 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
160
Q

Describe varicella/herpes zoster virus infection in pregnancy

A
  • 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
161
Q

Describe rubella infection in pregnancy

A
  • Background: usually affects children with mild illness and macular rash, but congenital rubella is rare due o 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
162
Q

Describe parvovirus B19 infection in pregnancy

A
  • 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
163
Q

Describe hepatitis infection in pregnancy

A
  • 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
164
Q

Describe HIV infection in pregnancy

A
  • 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
165
Q

Describe neural tube defects

A
  • 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)
166
Q

Describe abdominal wall defects

A
  • 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
167
Q

Describe urinary infections in pregnancy?

A
  • 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
168
Q

Describe the risks of obesity in pregnancy

A
  • 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
169
Q

Describe sickle cell disease in pregnancy

A
  • 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
170
Q

Describe antiphospholipid syndrome in pregnancy

A
  • Presence of lupus anticoagulant and/or anticardiolipin antibodies
  • Results in thrombotic events, which lead to recurrent miscarriages, IUGR, pre-eclampsia
171
Q

What are the different types of multiple pregnancies?

A
  • 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)
172
Q

What are the complications of multiple pregnancies?

A
  • 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
173
Q

What is the management of multiple pregnancies?

A
  • 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

Phase 3a (10 decks)

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