Obstetrics Flashcards

1
Q

Define and differentiate between gravidity and parity

A
  • Gravidity: total number of pregnancies, regardless of outcome
  • Parity: Total number of pregnancies carried over threshold of viability (24+0 in UK)

Examples

  • Patient is currently pregnant; had two previous deliveries = G3 P2
  • Patient is not pregnant, had one previous delivery = G1 P1
  • Patient is currently pregnant, had one previous delivery and one previous miscarriage = G3 P1+1 (the +1 refers to a pregnancy not carried to 24+0).
  • Patient is not currently pregnant, had a live birth and a stillbirth (death of fetus after 24+0) = G2 P2
  • Patient is not pregnant, had a twin pregnancy resulting in two live births = G1 P1
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2
Q

What is cardiotocography and how does it work

A
  • A way to record fetal heartbeat and uterine contractions during pregnancy
  • Does this by measuring tension of the maternal abdominal wall which provides indirect indication of intrauterine pressure
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3
Q

What is the normal foetal heart rate

A

100-160 bpm

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4
Q

When is CTG commonly used

A

If the fetal heart rate pattern (baseline tachycardia or bradycardia or decelerations) is not normal and suggest fetal distress or an increased risk of fetal distress, continuous monitoring with a CTG is indicated if this is available. A CTG will help decide whether fetal distress is present or not. It will also help identify fetal distress if it does develop later in labour. There is no need for routine continuous CTG monitoring in low risk labours if the fetal heart rate pattern is normal when assessed with a fetal monitor.

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5
Q

How do you interpret a CTG

A

DR C BRaVADO

  • Define Risk
  • Contractions
  • Baseline Rate
  • Variability
  • Acceleration
  • Deceleration
  • Overall impression
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6
Q

What is the relevance of defining risk in a CTG interpretation

A
  • Context to CTG reading
  • Threshold for intervention varies as risk is high or low
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7
Q

How do you assess contractions on CTG

A
  • Assess number of contrations in 10 minutes
    • Square = 1 minute
  • Assess:
    • Duration of contraction
    • Intensity
      • Assessed using palpation
  • Eg 2 in 10 minutes (or 2 in 10)
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8
Q

What are some factors that define the pregnancy as high risk

A

Maternal Medical Illness

  • Gestational Diabetes
  • Hypertension
  • Asthma

Obstetric Complications

  • Multiple gestation
  • Post-date gestation
  • Previous C-section
  • IUGR
  • Premature rupture of membranes
  • congenital malformations
  • Oxytocin induciton/augmentation of labour
  • Pre-eclampsia

Other Risk Factors

  • Absence of prenatal care
  • Smoking
  • Drug abuse
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9
Q

How do you assess baseline rate of fetal heart

A
  • Average HR of foetus within 10 minutes
  • Ignore decelerations or accelerations
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10
Q

Define Fetal tachycardia and name some causes

A

HR > 160 bpm

  • Fetal hypoxia
  • Chorioamnionitis
  • Hyperthyroidism
  • Fetal or maternal anaemia
  • Fetal tachyarrhythmia
  • Prematurity
  • Maternal pyrexia
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11
Q

Define fetal bradycardia

A

HR < 100 bpm

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12
Q

It is common to have a baseline HR of 100-120bpm in which two situations

A
  • Post-date gestation
  • Occiput posterior or transverse presentations
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13
Q

Define severe prolonged bradycardia. What does this indicate

A

HR < 80 bpm for more than 3 minutes

Severe fetal hypoxia

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14
Q

What are some causes of prolonged severe bradycardia

A
  • Prolonged cord compression
  • Cord Prolapse
  • Epidural and spinal anaesthesia
  • MAternal seizures
  • Rapid fetal descent
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15
Q

How can variability be categorised

A
  • Reassuring: 5-25 bpm
  • Non-reassuring
    • <5 bmp for 30-50 min
    • >25 bmp for 15-25 min
  • Abnormal
    • <5 bpm for >50 min
    • >25 bpm for >25 min
    • Sinusoidal
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16
Q

What are some causes of reduced variability on a CTG

A
  • Fetal sleeping - no longer then 40 minutes
    • Most common
  • Fetal acidosis (due to hypoxia)
    • More likely if late decelerations also preent
  • Fetal tachycardia
  • Drugs
    • Opiates
    • Benzodiazepines
    • Methyldopa
    • Magnesium sulphate
  • Prematurity
    • <28 weeks
  • Congenital heart abnormalities
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17
Q

Define an acceleration on CTG and is this reassuring or not

A
  • Abrupt increase in HR of more than 15 bpm for >15 seconds
  • reassuring
  • Accelerations alongside uterine contractions is a sign of healthy featus
  • Absence of acceleration with an otherwise normal CTG is of uncertain significance
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18
Q

Define variability on CTG and what does information does it tell tyou

A
  • Variatioin of fetal HR from one beat to the next
    • Variability occurs as a result of interaction between nervous system, chemoreceptors, baroreceptors and cardiac responsiveness,
  • Good incicator of how healthy a fetus is at a particular moment in time, as a healthy fetus will be able to adapt its HR in response to environment
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19
Q

Normal variability range on CTG

A

5-25 bmp variability

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20
Q

Describe features of early deceleration

A
  • Early decelerations start when uterine contractions begin and recover when contractions stop
  • Increased detal intracranial pressure -> increased vagal tone
    • So quickly resolves as ICP reduces when contraction ends
  • Physiological and NOT pathological
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21
Q

Describe features of variable deceleration

A
  • Rapid fall in baseline HR with variable recovery phase
  • Variable in duration and may not have any relationship to unterine contractions
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22
Q

How does umbilical cord compression lead to variable decelerations

A
  • The umbilical vein is often occluded first causing an acceleration in response.
  • Then the umbilical artery is occluded causing a subsequent rapid deceleration.
  • When pressure on the cord is reduced another acceleration occurs and then the baseline rate returns.
  • Accelerations before and after a variable deceleration are known as the “shoulders of deceleration”.
  • Their presence indicates the fetus is not yet hypoxic and is adapting to the reduced blood flow.
  • Variable decelerations can sometimes resolve if the mother changes position.
  • The presence of persistent variable decelerations indicates the need for close monitoring.
  • Variable decelerations without the shoulders are more worrying, as it suggests the fetus is becoming hypoxic.
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23
Q

Describe features of late deceleration and what does it indicate

A
  • Start at the peak of contraction and recover after it ends
  • Indicates insufficient blood flow to uterus and placenta
    • Blood flow to fetus sig reduced causing fetal hypoxia and acidosis
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24
Q

What are some causes of reduced uteroplacental blood flow (which results in late decelerations)

A
  • Maternal HYPOtension
  • Pre-eclampsia
  • Uterine hyperstimulation
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25
Q

Define prolonged deceleration on CTG

A
  • Prolonged deceleration is a deceleration that lasts more than 3 minutes
    • Non-reassuring 2-3 minutes
    • Abnormal > 3 mintues
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26
Q

Describe features of sinusoidal patterns on CTG

A
  • RARE but concerning - high fetal morbidity and mortality
    • Smooth, regular wave-like pattern
    • Frequency of 2-5 cycles a minute
    • Stable baseline around 120-160 bpm
    • NO beat to beat variability
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27
Q

Define a deceleration on a CTG a

A
  • Abrupt decrease in fetal HR of more than 15 bpm for more than 15 sec
  • The fetal heart rate is controlled by the autonomic and somatic nervous system. In response to hypoxic stress, the fetus reduces its heart rate to preserve myocardial oxygenation and perfusion. Unlike an adult, a fetus cannot increase its respiration depth and rate. This reduction in heart rate to reduce myocardial demand is referred to as a deceleration.
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28
Q

What are the types of deceleration on CTG

A
  • Early deceleration
  • Variable deceleration
  • Late deceleration
  • Prolonged deeleration
  • Sinusoidal
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29
Q

When are variable decelerations often seen nd usually caused by what

A

Often seen:

  • During labour and in patients with reduced amniotic fluid volume
  • Fetus experience stress during labour (reduced fetal perfusion as a result of uterine contractions)
  • Stress ie expected during labour but it is challenging to pick up pathological fetal distress
  • Caused usually by: umbilical cord compression
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30
Q

What does a sinusoidal pattern indicate

A
  • Severe fetal hypoxia
  • Severe fetal anaemia
  • Fetal/maternal haemorrhage
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31
Q

Late decelerations on CTG are a _____ finding and urgent _____ (investigation) is needed to assess for foetal _____ and _____. A pH of >_____ in labour is considered normal. Urgent delivery should be considered if there is foetal _____.

A

Late decelerations on CTG are a pathological finding and urgent foetal blood sample (investigation) is needed to assess for foetal hypoxia and acidosis. A pH of >7.2 in labour is considered normal. Urgent delivery should be considered if there is foetal acidosis.

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32
Q

NICE 2010: To reduce the risk of hypertensive disroders in pregnancy, what should women who are at high risk of developing HTN disorders (pre-eclampsia) be given (incl dose and duration)

A
  • Aspirin 75mg od from 12 weeks until birth of baby
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33
Q

What factors would rank a pregnant woman a high-risk for developing Hypertensive disorders (4)

A
  • Hypertensive disease during previous pregnancies
  • Chronic Kidney Disease
  • Autoimmune disorders (SLE or Anti-phospholipid syndrome)
  • Type 1 or 2 Diabetes Mellitus
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34
Q

Describe for blood pressure varies during normal pregnancy

A
  • BP usually falls in first trimester (particularly diastolic)
  • Continues to fall until 20-24 weeks
  • After this the BP usually increases to pre-pregnancy levels by term
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35
Q

How is hypertension defined in pregnancy

A
  • Systolic > 140 mmHg OR Diastolic > 90 mmHg -> Pre-eclampsia
  • OR increase above booking readings of:
    • >30 mmHg systolic or > 15 mmHg diastolic
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36
Q

What is the definitive treatment of pre-eclampsia

A

Deliver of baby

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37
Q

What is used as prophylaxis against seizures in pre-eclampsia and name a side effect

A
  • Magnesium Sulphate
  • Crosses placenta freely. Leads to self-limiting hypotonia in the neonate
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38
Q

Difference in BP between mild-?moderate and severe pre-eclampsia

A
  • Mild
    • >140 Systolic
    • >90 diastolic
  • Severe
    • >160 systolic
    • >110 diastolic
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39
Q

What is the treatment for a pregnant woman with severe pre-eclampsia

A

1st Line

  • IV Hydralazine and/or Labetalol* -> High to Low BP
    • HTN
  • IV magesium sulfate
    • seizure prophylaxis with
  • AIM: Get BP to 140-160 systolic and 90-110 diastolic
    • Severe systolic HTN leads to loss of cerebral vasculature auto-regulation

2nd line

  • Nicardipine and nifedipine PO
    • Calcium channel blockers

Short term/Emergency/Others have failed

  • IV Nitroglycerin
  • IV Sodium Nitroprusside.

* LAbetolol first line in NICE 2010

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40
Q

What is the first line treatment for pregnancy-induced hypertension (pre-eclampsia)

A

Labetolol

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41
Q

What are some considerations when considering to use sodium nitroprusside in severe hyeprtension of pregnancy

A
  • carefully monitored and reserved for extreme emergencies due to concerns about cyanide and thiocyanate toxicity in the mother and fetus,
  • as well as increased intracranial pressure in the mother
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42
Q

Define HELLP Syndrome

A

Pre-eclampsia with thrombotic microangiopathy involving the liver, characterised by:

  • Haemolytic anaemia
    • Low Hb, low Hct, high bilirubin, raised LDH, schistocytes on peripheral smear, dark urine
  • Elevated Liver Enzymes
    • Elevated AST/ALT, Epigastric pain, liver failure, abnormal clotting
  • Low Platelets

Warrants immediate delivery. Occurs in 10-20% of patients with pre-eclampsia

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43
Q

Clinical features of pre-eclampsia

A
  • Headache
  • Visual disturbances (scotoma)
  • Vomiting
  • Drowsiness
  • Epigastric/RUQ pain
  • Oedema
  • HTN
  • Proteinuria ++
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44
Q

Complications of pre-eclampsia

A

Maternal

  • Cerebrovascular accident
  • Eclampsia
  • Haemorrhage
    • Placental abruption
    • Intra-abdominal
    • Intra-cerebral
  • Multi-organ failure
  • Cardiac failure
    • Pulmonary oedema
    • Liver Failure
    • Renal Failure

Foetal

  • Prematurity
  • IUGR, growth retardation
  • Increased mortality/morbiditiy
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45
Q

Differential diagnoses for hypertension in pregnancy and how would you differentiate between each one

A
  • Chronic, pre-maternal hypertension
  • Gestational Hypertension
  • Chronic hypertension with superimposed pre-eclampsia
  • HELLP Syndrome
  • Pre-eclampsia
  • Eclampsia

Differentiate using:

  • Onset
  • Severity of HTN
  • Proteinuria
  • Oedema
  • RUQ pain
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46
Q

Define Chronic hypertension with superimposed pre-eclampsia

A
  • characterized by isolated hypertension before 20 weeks’ gestation with development of additional signs of preeclampsia after 20 weeks’ gestation.
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47
Q

What are patients with pre-eclampsia at risk of developing in the future

A
  • four-fold increased risk of developing hypertension later in life
  • two-fold increased risk of ischemic heart disease, stroke, and venous thromboembolism.
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48
Q

What are the features of magnesium toxiity

A
  • Somnolence (hypersomnia)
  • Absent deep tendon reflexes
  • Hypotension
  • Bradycardia
  • ECG changes
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49
Q

What is the antidote for magneium sulphate toxicity

A

. Calcium gluconate infusion

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50
Q

How is a diagnosis of pre-eclampsia made

A

Mild preeclampsia

  • Two serial blood pressure readings of >140/90 mmHg (either systolic or diastolic) over four hours or more AND
  • >0.3 g/24hrs of protein in the urine.

Preeclampsia is considered severe with blood pressure of >160/110 mmHg (either systolic or diastolic), urinary protein of >5g/day, or if there are signs of end-organ damage such as visual disturbance, hepatocellular injury, thrombocytopenia, oliguria (<500mL produced per day), fetal growth restriction, or pulmonary edema.

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51
Q

With pre-eclampsia what are the options for timing of birth (i.e. when should you deliver and any considerations)

A

Before 34 weeks (33+6)

  • Continue surveillance unless there are indications for planned early birth.
  • Offer intravenous magnesium sulfate and a course of antenatal corticosteroids in planned early birth

34 to 36+6 weeks

  • Continue surveillance unless there are indications for planned early birth
  • When considering the option of planned early birth, take into account the woman’s and baby’s condition, risk factors (such as maternal comorbidities, multi-fetal pregnancy) and availability of neonatal unit beds. Consider a course of antenatal corticosteroids in line with the NICE guideline on preterm labour and birth.

37 weeks onwards

  • Initiate birth within 24–48 hours.
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52
Q

What are some indications/thresholds for considering a planned early birth before 37 weeks in women with pre-eclampsia

A
  • Inability to control maternal BP despite using 3 or more classes of anti-hypertensives
  • Maternal O2 sats <90%
  • Progressive detrioration in liver funciton, renal function, haemolysis or platelet count
  • Ongoing neurological features (severe intractable headache, repeated visual scotoma, eclampsia)
  • Placental abruption
  • Reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring cardiotocograph pr stillbirth

MDT: Senior obstetrician, anaesthetic team, neonatal team.

OFFER: Magnesium sulfate and course of antenatal corticosteroids if planned early birth

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53
Q

Featueres of pre-existing hypertension in pregnancy

A
  • H of HTN before pregnancy
    • > 140/90 mmHg before 20 weeks gestation
  • No proetinuria
  • No oedema
  • 3-5% pregnancies and more common in older women
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54
Q

Features of pregnancy-induced hypertension (PIH or gestational HTN)

A
  • HTN occuring in second half of pregnancy (>20 weeks gestation)
  • No proteinuria
  • No oedema
  • 5-7% pregnancies
  • Resolves following birth (typically after 1 month)
  • These women are at increased risk of furute pre-eclampsia or HTN in later life
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55
Q

Features of pre-eclampsia

A
  • Pregnancy-induced HTN
  • Proteinuria (>0.3g/24hrs)
  • Oedema but less commonly used as criteria
  • 5% pregnancies
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56
Q

What are some moderate and high risk factors of pre-eclampsia

A

Moderate RF:

  • First pregnancy
  • Multiple pregnancy
  • ≥ 40 years
  • Pregnancy interval of >10 years
  • BMI ≥ 35 at first visit
  • FH

High RF:

  • HTN disease in previous pregnancy (PreE, E, HELLP, gHTN)
  • Chronic Kidney Disease
  • Autoimmune disease (SLE, Anti-phospholipid syndrome
  • T1DM, T2DM
  • Chronic HTN
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57
Q

Features of severe pre-eclampsia

A
  • HTN >160/110 mmHg
  • Proteinuria dipstick ++/+++
  • Headache
  • Visual disturbance
    • Scotoma
  • Papilloedema
  • RUQ/epigastric pain
  • Hyperreflexia
  • Low Plt, abnormal LFT, HELLP
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58
Q

Define eclampsia

A
  • Development of seizures in association with pre-eclampsia:
    • symptoms >20 weeks gestation
    • Pregnancy-induced HTN
    • Proteinuria
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59
Q

What is the treatment and preventor of eclampsia

A
  • IV Magnesium Sulfate
    • Eclampsia: IV bolus 4g over 5-10 minutes, followed by infusion of 1g/hour
  • Monitor:
    • Urine output, reflexes, respiratory rate and O2 sats
      • Respiratory depression as result of Mg toxicity
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60
Q

How long should treatment continue after a seizure in eclampsia

A
  • Continue for 24 hours after last seizure or delivery
    • 40% seizures occur post-partum

NB: severe pre-eclampsia/eclampsia - fluid restrict to prevent fluid overload

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61
Q

Define amniotic fluid embolism

A
  • Foetal cells/amniotic fluid (liqour) enters maternal bloodstream
  • Stimulates reaction which results in anaphylaxis - obstetric emergency

Rare complication of pregnancy. High mortality rate. Incidence 2 per 100,000 UK.

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62
Q

What are some risk factors for amniotic fluid embolism

A
  • Maternal Age
  • Induction of labour

Many associated RF - multiple and prevention is impossible. Aetiology not been proven but widely accepted concept that maternal circulation must be exposed to liqour

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63
Q

When does amniotic fluid embolism typically present

A
  • Majority in labour
  • Caeserian sections
  • Immediate post-partum
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64
Q

What ar th signs and suymptoms of amniotic fluid embolsm

A

Signs

  • Cyanosis
  • LOW BP
  • Bronchospasms
  • HIGH HR
  • Arrhythmia
  • Myocardial infarction

Symptoms

  • Chills
  • Shivering
  • Sweating
  • Anxiety
  • Coughing
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65
Q

How is amniotic fluid embolism diagnosed

A
  • Clinical diagnosis of exclusion
    • No definitive diagnostic tests
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66
Q

MAnagement of amniotic fluid embolism

A
  • Critical care unit by MDT
  • Supportive management iwth resuscitation
    • Blood (FBC, clotting, U&E, cross match)
    • Treatment of massive obstetric haemorrhage
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67
Q

When should a woman be assessed for her risk of venous thromboembolism (VTE)

A
  • At booking (8-12 weeks)
  • Subsequent hospital admission
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68
Q

What risk factors are assessed at booking for VTE

A
  • >35 year
  • BMI > 30
  • Parity > 3
  • Smoker
  • Gross varicose veins
  • Current pre-eclampsia
  • Immobility
  • FH of unprovoked VTE
  • Low risk thrombophilia
  • Multiple pregnancy
  • IVF pregnancy
  • Hospitalisation
  • Anaesthesia
  • Central venous catheter: Femoral >> Subclavian
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69
Q

With risk factors in mind, when would you prophylactically treat someone for VTE

A
  • ≥4 RF warrants immediate treatment with LMWH until 6 weeks post-natal period
  • 3 RF LMWH initiated at 28 weeks and continued until 6 weeks post-natal
  • If DVT diagnosed shortly before delivery
    • continue anti-coagulation treatment for at least 3 months (as in other patients qwith provoked DVTs)

Pregnant woman with previous VTE history is considered high risk immediately and requires immediate LMWH throughout antenatal period

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70
Q

What is the prophylactic treatment of VTE in pregnancy

A
  • Low Molecular Weight Heparin (LMWH)
  • DO NOT GIVE:
    • Direct Oral Antigocaulants (DOACs)
    • Warfarin
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71
Q

What are some underlying medical conditions that predisposes VTEs

A
  • Pregnancy
  • Malignancy
  • Thrombophilia
    • Activated protein C Rsistance, Protein C and S deficiency
  • Heart failure
  • Anti-phospholipid syndrome
  • Behcet’s
  • Polycythaemia
  • Nephrotic syndrome
  • Sickle cell disease
  • Paroxysmal nocturnal haemoglobinuria
  • Hyperviscosity syndrome
  • Homocystinuria
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72
Q

What are some medications that predisposes you to VTE

A
  • COCP
    • 3rd generation >> 2nd generation
  • HRT
    • O+P >> O only
  • Raloxifene
  • Tamoxifen
  • Antipsychotics (Onlazapine)
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73
Q

In obstetric cholestasis, what is there an increased risk of (2)

A
  • Premature birth
  • Still birth
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74
Q

Features of obstetric cholestasis

A
  • Pruritis
    • ​Palms, soles, abdomen
  • Raised bile acids
  • Bilirubin and LFT may be elevated
    • 20% are clinically jaundiced
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75
Q

Management of obstetric cholestasis

A
  • Induction of labour at 37 weeks
    • Common practice but not really evidence based
  • Ursodeoxycholic acid (UDCA)
    • Used but not clear
  • Vitamin K supplementation
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76
Q

Which systems are affected phsyiologically during pregnancy

A
  • Cardiovascular
  • Repiratory
  • Blood
  • Urinary
  • Biochemical changes
  • Liver
  • Uterus
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77
Q

What are some cardiovascular changes seen in pregnancy

A
  • Increased:
    • SV (130%)
    • HR (115%)
    • CO (140%)
  • Diastolic BP reduces in 1st and 2nd trimester
    • Returns to non-pregnant levels by term
  • Enlarged uterus -> venous return disruption
    • Ankle oedema
    • Supine hypotension
    • Varicose veins
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78
Q

What are some respiratory changes seen in pregnancy

A
  • Increased
    • Ventilation (140%)
    • Tidal volume 500-700mL
      • Progesterone on respiratory centre
    • Oxygen requirement (120%)
      • Overbreathing leads to reduced pCO2
      • Give rise to ‘dyspnoea’
    • Basal metabolic rate (115%)
      • Increased thyroxine and adrenocrotical hormone
      • Find warm conditions uncomfortable
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79
Q

What are some haematological changes in pregnancy

A
  • Mild Anaemia
    • Increased Red cell mass (120-30%)
    • Plasma volume increase (150%)
      • Net dilution
    • Macrocytosis
      • Normal
      • Folate or B12 deficiency
  • Neutrophilia
  • Thrombocytopenia
    • Increased platelet size
  • Increase fibrinogen and Factors VII, VIII, X
    • Low grade increase in coagulant activity
    • Decreased fibrinolysis
      • Returns to normal after delivery (?placental disruption)
    • Increased risk VTE
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80
Q

What are some changes in the urinary system seen in pregnancy

A
  • Increased
    • Perfusion (130%)
    • GFR (130-60%)
    • Salt and water reabsorption
      • Elevated sex steroid levels
    • Urinary protein loss
      • >300mg/24hrs in pregnant women
      • >150mg/24hrs in non-pregnant
      • Cautious as sign of pre-eclampsia
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81
Q

What biochemical changes are seen in pregnancy

A
  • Increased
    • Calcium requirements
      • Esp 3rd trimester up until lactation
      • Ca transported actively acorss placenta
    • Gut absorption of Ca
      • Increased 1,25 Vit D
    • Ionised Ca stable
  • Decreased
    • Serum Ca and Pi
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82
Q

What are some liver changes seen during pregnancy

A
  • NO CHANGE in hepatic blood flow (unlike renal and uterine)
  • Raised ALP (150%)
  • Decreased albumin
    • Dilutational?
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83
Q

What changes are seen in the uterus during pregnancy

A
  • Increase
    • Mass 100g -> 1100g
    • Hyperplasia THEN hypertrophy
    • Cervical ectropion and discharge
  • Braxton-Hicks
    • Non-painful practice contractions late pregnancy (>30weeks)
  • Retroversion mar lead to retention (12-16weeks) usually self corrects
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84
Q

Pathophysiology of Rhesus disease

A
  • Rh -ve mother can develop anti-D igG antibodies if they deliver a Rh +ve child
  • Fetal blood may leak and cause above reaction
  • In later pregnancies, these IgG can cross placenta and cause haemolysis in the foetus
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85
Q

How is Rhesus disease prevented

A
  • Test for D antibodies in Rh -ve mothers at booking
    • Test Rhesus status
  • NICE (2008): anti-D to non-sensitised Rh -ve mothers at 28 and 24 weeks
  • RCOG (2011) - single dose (28wks) or double does (28 and 24 weeks)
  • If traumatic event is in 2nd/3rd trimester, give large dose of anti-D and perform Kleihauer test
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86
Q

What is the Kleihauer test

A
  • Determines proportion of fetal RBCs present if traumatic event happens 2nd/3rd trimester
  • Would also give big dose of anti-D
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87
Q

Anti-D Immunoglobulin should be given (ALWAYS within 72 hours) in what situations

A
  • Delivery of Rh +ve infant, live or stillborn
  • Termination of pregnancy
  • Miscarriage (if gestation > 12 weeks)
  • Ectopic pregnancy surgical management
    • Not required if managed with methotrexate
  • External cephalic version
  • Antepartum haemorrhage
  • Amniocentesis, chorionic villus sampling, fetal blood sampling
  • Abdominal trauma
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88
Q

What tests are done in rhesus disease and what are their functions

A
  • FBC, blood group, Coomb’s test
    • All babies born to Rh -ve mothers - cord blood at delivery
  • Kleihauer test
    • Add acid to maternal blood, fetal cellls are resistant
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89
Q

What can happen to the fetus if they are affected in Rhesus disease

A
  • Oedematus
    • Hydrops fetalis
    • As liver devoted to RBC production, albumin falls
  • Jaundice, anaemia, hepatosplenomegaly
  • Heart failure
  • Kernicterus
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90
Q

Treatment of affected fetus in rhesus disease

A
  • Transfusions
  • UV phototherapy
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91
Q

Define placenta praevia

A
  • When the placenta implants in the lower uterus close to or covering the internal cervical os.
  • 5% will have low lying placenta when scanned at 16-20 weeks gestation
  • Incidence at delivery is 0.5% therefore most placentas rise away from cervix

IMPORTANT CAUSE OF ANTEPARTUM HAEMORRHAGE

DEATH NOW EXTREMELY RARE. Major cause of death in women with placenta praevia is now PPH

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92
Q

List and describe the different types of placenta praevia

A
  • Complete
    • Completely covers cervical os
  • Partial
    • Partially covers cervical os
  • Marginal
    • Edge of placenta extends to within 2cm of cervical os
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93
Q

Define the classical grading for placenta praevia

A
  • I - placenta reaches lower segment but not the internal os, extends within 2cm of os
  • II - placenta reaches internal os but doesn’t cover it
  • III - placenta covers internal os before dilation but not when dilated
  • IV - placenta completely covers the internal os
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94
Q

What are some risk factors for placenta praevia

A

Anything that has damaged endometrium and decrease vascularisation

  • Previous C-section
  • Abortion
  • Uterine surgery
  • Multiparity
  • Multiple pregnancies

Other

  • Multiple placentas
  • Placenta with larger than normal SA
    • Twins or triplets
  • Maternal age > 35
  • Intrauterine fibroids
  • Maternal smoking
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95
Q

Clinical features of placenta praevia

A
  • NO pain and uterus NOT tender
  • Lie and presentation may be abnormal
  • Fetal heart usually normal
  • Small bleeds before large
  • Shock proportional to visible loss
  • Coagulation problems rare
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96
Q

Investigations for placenta praevia

A
  • Often picked up at routine check up >20 weeks on abdominal US
  • RCOG = transvaginal ultrasound to localise placenta
    • If placenta praevia is possible diagnosis, digital vaginal examination should not be performed until placenta praevia has been excluded -> cause bleed

Could also speculum to check for polyps/ectropion

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97
Q

What are the two contexts which would change how you manage placenta praevia

A
  • If low-lying placenta at 16-20 week scan OR
  • Placenta praevia with bleeding
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98
Q

In patient who has a low lying placenta in their 16-20 week scan, what would your management be

A
  • Rescan at 34 weeks
    • No need to limit activity or intercourse UNLESS THEY BLEED
  • If still present at 34 weeks and grade I or II:
    • Scan every 2 weeks
  • If high presenting part or abnormal lie at 37 weeks
    • C-section deliverr
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99
Q

In patient who has placenta praevia with bleeding, what would your management be

A
  • Admit
  • Treat shock
  • Cross match blood
  • Find ultrasound at 36-37 weeks to determine method of delivery:
    • C-section: Grade II or IV at 37-38 weeks
    • Vaginal delivery: Grade I
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100
Q

What are the two causes of jaundice in pregnancy

A
  • Intrahepatic cholestasis of pregnancy (Obstetric cholestasis)
  • Acute fatty liver of pregnancy
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101
Q

What is the most common liver disease of pregnancy

A

Obstetric cholestasis

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102
Q

When does obstetric cholestasis typically present

A

Third trimester

Occurs in 1% pregnancies

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103
Q

Features of obstetric cholestasis

A
  • Pruritis (severe), in palms and soles
  • No rash (skin changes due to scratching may be present)
  • Raised bilirubin
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104
Q

Management of obstetric cholestasis

A
  • Ursodeoxycholic acid
    • Symptomatic relief
  • Weekly LFTs
  • Induction of labour at 37 weeks
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105
Q

Comp[lications of obstetric cholestasis

A
  • Increased rate of stillbirth
  • Not generally associated with increased maternal morbidity
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106
Q

When does acute fatty liver of pregnancy usually present

A
  • Third trimester OR
  • Period immediatelty following delivery
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107
Q

Features of acute fatty liver of pregnancy

A

Non-specific presenting symptoms

  • Abdominal pain
  • Nausea and vomitting
  • Headache
  • Jaundice
  • Mild pyrexia
  • Hyupoglycaemia
  • Severe disease may result in pre-eclampsia

OBSTETRIC EMERGENCY

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108
Q

Investigations for acute fatty liver of pregnancy (AFLP)

A
  • Elevetaed transaminases (ALT >500 u/L)
  • Investigate synthetic function of liver (clotting studies)
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109
Q

Management of acute fatty liver of pregnancy

A
  • Supportive care
  • Once established delivery is definitive management
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110
Q

Name the three conditions under the spectrum Gestational trophoblastic disorders

A

Disorder originating from placental trophoblast

  • Complete hydatidiform mole
  • Partial hydatidiform mole
  • Choriocarcinoma
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111
Q

What is the underlying pathology in complete hydatidiform mole

A
  • Benign tumour of trophoblastic material
  • When empty egg is fertilised by single sperm
  • Sperm DNA replicated so all 46 chromsomes are paternal origin
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112
Q

Features of complete hydatidiform mole

A
  • Bleeding in first or early second trimester
  • Exaggerated symptoms of pregnancy (Hyperemesis)
  • Uterus large for dates
  • Very high levels of hCG
  • Hypertension and hyperthyroidism may be seen
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113
Q

Why could hypertension and hyperthyroidism be seen in complete hydatidiform mole pregnancies

A
  • Beta hCG similar in structure to LH, FSH and TSH
  • so B-hCG can stimulate thyroid production of thyroxine (T4) and triiodothyronine (T3)
  • T4 and T3 have negative feedback on pituitary gland leading to fall in TSH levels
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114
Q

In complete hydatidiform molar pregnancy, what would you expect the B-hCG, TSH and thyroxine levels to be

A
  • High B-hCG
  • High thyroxine
  • Low TSH
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115
Q

Management of complete hydatidiform molar pregnancy

A
  • URGENT referal to specialist centre
    • Evacuation of uterus is performed
  • Contraception is recommended to avoid pregnancy in the next 12 months

around 2-3% develop choriocarcinoma

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116
Q

What is the underlying pathology in partial mole

A
  • Normal haploid egg may be fertilised by two sperms or by one sperm with duplication of paternal chromosomes
  • DNA is maternal and paternal in origin
  • Usually triploid 69 XXX or 69 XXY
  • Feotal parts may be seen
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117
Q

Describe the stages of labour with some details on timing

A
  • Initiation and diagnosis of labour
    • Braxton Hicks contractyions in third trimester which develop into contraction
    • Labour diagnosed when there are painful regular contractions which lead to effacement and dilatation of cervix
  • First Stage
    • From diagnosis of labour to full dilation of cervix (10cm)
    • Membranes rupture now normally, if not already
    • Latent phase: Cervix dilates slowly for first 4 cm - takes several hours
    • active phase: 1cm/h dilatation nulliparous women or 2cm/hr in multiparous
    • Active first stage should NOT last more tha 16 hours
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118
Q

How is labour diagnosed

A
  • Initiation and diagnosis of labour
    • Braxton Hicks contractyions in third trimester which develop into contraction
    • Labour diagnosed when there are painful regular contractions which lead to effacement and dilatation of cervix
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119
Q

What happens in the first stage of labour (description and baby movement) and how long should this last

A

From diagnosis of labour to full dilation of cervix (10cm)

  • Descent, flexion and internal rotation occur to varying degrees
  • Membranes rupture now normally, if not already
  • Latent phase: Cervix dilates slowly for first 4 cm - takes several hours
  • active phase: 1 cm/hr dilatation nulliparous women or 2 cm/hr in multiparous
  • Active first stage should NOT last more than 16 hours
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120
Q

What happens in the second stage of labour and how long does this usually last

A

From full dilatation of cervix to delivery of baby

  • Descent flexion and rotation are copmleted and followed by extension as head delivers
  • Passive stage: Full dilatation until head reaches pelvic floor and mother has desire to push.
    • Rotation and flexion are commonly completed here
    • May last a few minutes but can last longer
  • Active stage: When mother is pushing
    • Pressure of head on pelvic floor produces irresistable desire to bear down (epidural may prevent this)
    • bBaby deliveres after 40 minutes (nulliparous) or 20 minutes (multiparous)
    • Can be quicker but if it takes >1 hours, SVD becomees increasingly unlikely
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121
Q

Describe the movements involved at delivery (ie as babies head extends out of poerineum)

A
  • Head extends out through perineum and out of the pelvis
  • Perineum stretches and often tears (episiotomy)
  • Head restitues and rotates 90o to adopt transvere position (same position as it entered the pelvic inlet)
  • Shoulders deliver in the next contraction
    • Anterior shoulder comes under symphysis pubis first, then posterior shoulder then rest of body (see pg 285 for more detail)
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122
Q

What happens in the third stage of labour

A

Time of delivery to delivery of placenta

  • Uterine muscle fibres contract to compress blood vessels supplying placenta
  • This hears away from uterine wall and is delivered
  • Lasts 15 minutes
  • Normal blood loss up to 500 mL
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123
Q

Describe the pathology in placenta accreta

A
  • Attachment of the placenta to the myometrium due to defective decidua basalis.
  • Placenta does not properly separate in third stage of labour -> risk of PPH
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124
Q

Risk factors for placenta accreta

A
  • Previous c-section
  • Placenta praevia
  • PID
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125
Q

Describe the three types of placent accreta

A
  • accreta: chorionic villi attach to the myometrium, rather than being restricted within the decidua basalis
  • increta: chorionic villi invade into the myometrium
  • percreta: chorionic villi invade through the perimetrium
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126
Q

Define shoulder dystocia

A
  • Complication of vaginal cephalic delivery
  • Inability to deliver the body of the foetus using gentle traction, the head already being delivered
  • Usually due to anterior foetal shoulder impacting on maternal symphysis pubis
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127
Q

What are some risk factors for shoulder dystocia

A

Fetal

  • Macrosomia

Maternal

  • High BMI
  • Diabetes Mellitus
  • Prolonged labour (second stage?)
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128
Q

What are some maneouvres used in shoulder dystocia

A
  • ASK FOR HELP as soon as shoulder dystocia identified
  • McRobert’s maneouvre performed, if unsuccessful:
    • Can use the woodscrew maneouvre
    • Rubin maneouvre
    • Mother on all fours on all fours
  • If nothing works Push head back and do emergency c-section
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129
Q

What is McRoberts Position

A
  • Hyperflexion and abduction of mother’s hips, with her thighs towards her abdomen
  • Apply suprapubic pressure
  • This rotation increases the relative anterior-posterior angle of the pelvis and often facilitates a successful delivery
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130
Q

What is Rubin maneouvre

A
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131
Q

What is woodscrew maneouvre

A
  • Putting hand in the vagina to attempt to rotate baby 180 degrees
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132
Q

What is the Zavanelli maneuver

A

Cephalic replacement via reversal of the cardinal movements of labour

Not first-line option

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133
Q

Folic acid supplementation is important in preventing what

A

Formation of neural tube defects

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134
Q

How does folic acid function in foetal development

A
  • Folic acid converted to tetrahydrofolate (THF).
  • Role in transfer of 1-carbon unite (methyl etc) to essential substrates involved in DNA and RNA synthesis
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135
Q

Source of folic acid

A

Supplementation

Green leafy vegetables

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136
Q

Causes of folic acid deficiency

A
  • Phenytoin
  • Methotrexate
  • Pregnancy
  • EtOH excess
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137
Q

Consequences of folic acid deficiency

A
  • Macrocytic , megaloblastic anaemia
  • Neural tube defects
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138
Q

What is the recommendation with preventing neural tube defects during pregnancy

A
  • ALL women should take 0.4mg (400mcg) folic acid/day pre-conception and continue until 13 weeks
    • Started pre-conception as neural tube forms within first 28d of embryo development
  • Women at high risk of conceiving a child with NTD should take 5 mg/day pre conception until 12th week pregnancy
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139
Q

What factors would make a mother at high risk of conceiving a baby with NTD

A
  • Previous child with NTD (or FH)
  • Diabetes mellitus
  • Anti-epileptic
  • Obese (BMI >30)
  • HIV +ve taking co-trimoxazole
  • Sickle cell (thalassamie trait)
  • Coeliac disease (malabsorption)
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140
Q

Define lochia

A
  • Vaginal discharge containing blood, mucous and uterine tissue during puerperium
    • Period of 6 weeks after birth in which mother;s reproductive organs return to normal
    • L:ochia is normal part of this process
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141
Q

When would you start investigating lochia and how would you investigate

A

Ultrasound if lochia persists beyond 6 weeks

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142
Q

How would you counsel and safety net a mother about their lochia

A

Counsel

  • Lochia is normal bleeding post partum
  • Consists of blood, mucous and uterine tissue
  • Can pressit up to 6 weeks
  • Bright red first and then changes colour before finally stopping

Safety net to seek medical help if:

  • Offensive smell
  • Increase in volume
  • Or persists past 6 weeks
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143
Q

Define preterm prelabour rupture of the membranes (PPROMs)

A
  • Membranes rupture < 37 weeks
  • Aetiology often unknown but all causes of pre-term labour may be implicated
  • Occurs in 2% pregnancies but make up around 40% of preterm deliveries
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144
Q

What are some causes of preterm deliveries

A

Too much inside

  • Multiple pregnancy
  • Antepartum haemorrhage
  • Polyhydramnios

Defenders escape (foetal survival repsponse)

  • Antepartum haemorrhage
  • IUGR
  • Pre-eclampsia
  • Foetal distress (?)

Weak wall

  • Cervical incompetence
  • Uterine abnormalities

Other (Enemy)

  • Infection
  • Diabetes
  • Idiopathic
  • Iatrogenic
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145
Q

Complications of PPROM

A

Foteal

  • Preterm delivery (within 48hrs in 50% cases)
  • Infection
    • Funisitis (cord infeciton)
  • Pulmonary hypoplasia
  • Umbilical cord prolapse (rare)

Maternal

  • Chorioamnionitis
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146
Q

Clinical feature of PPROM (history)

A

History

  • Gush of clear fluid is normal
  • Followed by further leaking
  • <37 weeks gestation
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147
Q

Clinical featuers of PPROM (examination)

A
  • Sterile Speculum examination
    • Pool of fluid in posterior fornix is diagnostic - variable
  • AVOID DRE
    • Could cause infection
  • Features of chorioamnionitis
    • Contractions or abdominal pain
    • Fever or hypothermia
    • Tachycardia
    • Uterine tenderness
    • Coloured offensive liqour
      • Clinical signs often appear late
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148
Q

What investigations would you do in PPROM

A
  • Actim Partus
    • helps decide whether to send mother home or admit
  • USS
    • Reduced liqour (oligohydramnios) but can be normal as foetus produces urine
  • Look for infectyion
    • High vaginal swab
    • FBC
    • CRP
    • Lactate
  • CTG
    • Foetal well-being
    • Persistent tachycardia suggestive of infection
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149
Q

Management of PPROM

A
  • Admission
  • Regular observations to ensure chorioamnionitis is not developing
  • Oral erythromycin for 10 days
  • Antenatal corticosteroids
    • Reduce risk of RDS
    • Delivery considered at 34 weeks gestation
      • Trade off between risk of maternal chorioamnionitis with decrease risk of RDS in baby as pregnancy progresses
  • Co-amoxiclav CONTRAINDICATED as neonate prone to NEC
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150
Q

What are three mental health problems a mother might face post-partum

A
  • Baby blues
  • Postnatal depression
  • Peuperal psychosis
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151
Q

What are the differences in onset between babyblues, postnatal depression and peurperal psychosis

A
  • Baby Blues = 3-7d following birth, common in primimaprous mothers
  • Postnatl depression = month post-partum and peaks at 3 months
  • Peurperal psychosis = first 2-3 weeks following birth
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152
Q

Describe the differences in the clinical features of babyblues, postnatal depression and peurperal psychosis

A
  • Baby blues
    • Anxious, tearful and irritable
  • Postnatal depression
    • Similar to depression in other contexts (low mood, energy and anhedonia)
  • Peurperal psychosis
    • Severe mood swings (similar to bipolar disorder)
    • Disordered perception (auditory hallucinations)
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153
Q

Management of baby blues

A
  • Reassurance and provide support
  • Health visitor plays key role
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154
Q

Managment of postnatal depression

A
  • Reassurance and support as with baby blues
  • CBT first line!
  • Severe symptoms: SSRI (sertraline or paroxetine)
    • Secreted in breast milk but not harmful to babay
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155
Q

Managmeent of peurperal psychosis

A
  • Admission to hospital
  • 20% risk of recurrence following future pregnancies
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156
Q

When does the second screen for anaemia and atypical red cell alloantibodies occur in the entental care

A

28 weeks

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157
Q

When does nuchal scan occur in antenatal care

A

11 - 13 +6 weeks

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158
Q

When do you collect urine culture to detect asymptomatic bacteriuria

A

8-12 weeks (booking visit)

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159
Q

Describe the RCOG guidelines on grading perineal tears

A
  • 1st degree = Superficial damage with no muscle invovlement (not past fourchette)
  • 2nd degree = injury to perineal muscle but not involving anal sphincter
  • 3rd degree = injury to perineum involving anal sphincter complex
    • 3a = <50% of external anal sphincter thickenss torn
    • 3b = >50% EAS thickness torn
    • 3c = IAS torn
  • 4th degree = involves EAS and IAS AND rectal mucosa
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160
Q

Risk factors for perineal tears

A
  • Primigravida
  • Large baby (macrosomia)
  • Precipitant labour (very rapid childbirth 1st and 2nd stage labour < 2hours)
  • Shoulder dystocia
  • Forceps delivery
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161
Q

How do you differentiate between placenta praevia, placental abruption and vasa praevia

A
  • Placenta praevia = painless and bright red bleeding (usually small bleeds then large, with shock proportional to loss)
  • Placental abruption = associated with pain and dark red bleed
  • Vasa praevia = painless PV bleed + fetal bradycardia and membrane rupture
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162
Q

Define post-partum haemorrhage

A
  • Blood loss of >500mL
  • Primary = within 24hrs of delivery
  • Secondary = more than 24 hours -12 weeks post birth
    • Apparently changed from 6 weeks
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163
Q

What is the most common cause of PPH

A
  • Uterine atony (90% of cases)
  • Other causes:
    • Genital trauma
    • Clotting disorders (DIC or deficiencies)
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164
Q

Risk factors for primary PPH

A

Basically anything that causes distension of uterus or anything that stops it contracting

  • Previous PPH
  • Prolonged labour
  • Pre-eclampsia
  • Increased maternal age
  • Polyhydramnios
  • Emergency C-section
  • Placenta praevia
  • Placenta accreta
  • MAcrosomia
  • Ritodrine
    • B2 adrenergic receptor aghonist used for tocolysis

Previously thought multiparity was RF but recent modern studies show nulliparity is RF

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165
Q

Managment of PPH

A
  • Seek senior help! 222 call
  • ABC (+14G cannulae)
  • Medical
    • IV syntocinon 10 IU or IV ergomwetrine 500mcg
      • RCOG says 5 IU double check
    • IM carboprost
  • Surgical
    • Intrauterine balloon tamponade first line
      • Where uterine atony is only or main cause of haemorrhage
    • Others
      • B-Lynch suture
      • Ligation of uterine arteries orinternal iliac arteries
  • Severe haemorrhage
    • Hysterectomy = life-saving procedure
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166
Q

What is secondary PPH caused by

A
  • Retained placental tissue
  • Endometritis
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167
Q

What triad do women with preterm-PROM present with when they have chorioamnionitis

A
  • Maternal pyrexia
  • Maternal tachycardia
  • Fetal tachycardia

Reasonable differentials: PID, UTI (maybe STI)

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168
Q

What is the underlying pathology in chorioamnionitis

A
  • Ascending bacterial infection of amniotic fluid/membranes/placenta
  • Preterm premature rupture of membrane (however can still occur when membranes are intact) exposes sterile uterus to patohgens
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169
Q

Management of chorioamnionitis

A
  • Obstetric emergency
  • Prompt delivery of foetus (via c-section if necessary)
  • IV antibiotics initial treatment
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170
Q

Define placental abruption

A
  • Separation of normally sited placenta form uterine wall
  • results in maternal haemorrhage into intervening space

Occurs in ~1/200 pregnancies

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171
Q

What are some risk factors for placental abruption

A
  • Proteinuric hypertension
  • Multiparity
  • Maternal trauma
  • Increasing maternal age
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172
Q

What are some clinical features of placental abruption

A
  • Constant abdominal pain
  • Shock disproportionate to blood loss
    • 20% of placental abruptions are concealed - trapped behind placenta and doses not drain
  • Uterus may be in spasm and feel firm or woody
  • Fetal heart: absent or distressed
  • coagulation problems
  • Beware pre-eclampsia, DIC, anuria
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173
Q

Risk factors for Group B Streptococcus (GBS) infection inneonate

A
  • Prematurity
  • Prolonged rupture of membranes
  • Previous sibling with GBS infection
  • Maternal pyrexia (secondary to chorioamnionitis)
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174
Q

Management of GBS (RCOG 2017)

A
  • Universal screening for GBS should NOT be offered to all women
    • Maternal request is also NOT an indication for screening
  • Mothers who have had GBS detected in previous pregnancy should be informed of their risk of maternal GBS carriage (50%)
    • Offer maternal IV antibiotic prophylaxis (IAP)
    • OR testing in late pregnancy and then antibiotics if still positive
  • IAP
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175
Q

What are the indications for IV antibiotic prophylaxis (IAP)

A
  • Mother has GBS in previous pregnancy
  • Positive test in late pregnancy
  • Mothers with previous baby with earl- or late-onset GBS disease
  • Women in preterm labour - regardless of GBS status
  • Women with pyrexia during labour (>38)
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176
Q

What is the antibiotic of choice in GBS prophylaxis

A

Benzylpenicillin

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177
Q

What is the organism in GBS

A

Streptococcus agalactiae

Gram positive, coccus in chains, facilitative anaerobe

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178
Q

When should women have GBS swabs if they were to have swabs (ie if their previous pregnancy was GBS +ve)

A
  • 35-37 weeks OR
  • 3-5 weeks prior to anticipated delivery date
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179
Q

What organism causes ophthalmia neonatorum

A
  • Neisseria gonorrhoea
  • Gram negative diplococcus
  • Obligate anaerobe
  • Conjunctivites
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180
Q

Define oligohydramnios

A

Varied definitions

  • <500mL at 32-36 weeks AND
  • Amniotic Fluid Index (AFI) < 5th percentile
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181
Q

Causes of oligohydramnios

A
  • Premature rupture of membranes
  • Foetal renal problems (e.g. renal agenesis)
  • IUGR
  • Post-term gestation
  • Pre-eclampsia
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182
Q

What are three major causees of bleeding during pregnancy in the first trimester

A
  • Spontaneous abortion
  • Ectopic pregnancy
  • Hydatidiform mole

Exclude STIs and cervical polyps

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183
Q

What are three major causees of bleeding during pregnancy in the second trimester

A
  • Spontaneous abortion
  • Hydatidiform mole
  • Placental abruption

Exclude STIs and cervical polyps

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184
Q

What are four major causees of bleeding during pregnancy in the third trimester

A
  • Bloody show
  • Placental abruption
  • Placenta praevia
  • Vasa praevia

Exclude STIs and cervical polyps

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185
Q

Define antepartum haemorrhage

A

Bleeding after 24 weeks

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186
Q

Typically history of 6-8 weeks amenorrhoea with lower abdominal pain (usually unilateral) initially and vaginal bleeding later. Shoulder tip pain and cervical excitation may be present

Diagnosis?

A

Ectopic pregnancy

187
Q

Typically bleeding in first or early second trimester associated with exaggerated symptoms of pregnancy e.g. hyperemesis. The uterus may be large for dates and serum hCG is very high

Diagnosis?

A

Hydatidiform mole

188
Q

Constant lower abdominal pain and, woman may be more shocked than is expected by visible blood loss. Tender, tense uterus* with normal lie and presentation. Fetal heart may be distressed

Diagnosis?

A

Placental abruption

189
Q

Vaginal bleeding, no pain. Non-tender uterus* but lie and presentation may be abnormal

Diagnosis?

A

Placenta praevia

190
Q

Rupture of membranes followed immediately by vaginal bleeding. Fetal bradycardia is classically seen

Diagnosis?

A

Vasa praevia

191
Q

Should a vaginal exmination be performed (in primary care) for suspected antepartum haemorrhae

A

No

Can cause haemorrahge esp placenta praevia

192
Q

In a woman with epilepsey, risk of uncontrolled epilepsey during pregnancy generally outweigh risk of medication to the foetus. 2% risk of congenital defects in non-epileptic mothers and 4% in epileptic mothers. For each of the following AED, what congenital defects are they associated with:

  • Sodium valproate
  • Carbamazepine
  • Phenytoin
  • Lamotrigine
A
  • Sodium valproate - Neural tube defects and teratogenic
  • Carbamazepine - teratogenic (least of older AED)
  • Phenytoin - cleft palate
  • Lamotrigine -low rate of ocngenital malformations
193
Q

Is breastfeeding safe for mothers taking antiepileptics?

A

Yes

194
Q

Which AED is considered not safe when breastfeeding

A

barbiturates

195
Q

If a pregnant woman is taking phenytoin, what must be given in the last month of pregnancy to prevent clotting disorders in the newborn

A

Vitamin K

196
Q

What are some general diseases/disorders found in pregnancy

A
  • Pre-eclampsia/Eclampsia
  • Hypertension
  • Diabetes and GDM
  • Cardiac Disease
  • Respiratory disease
  • Epilepsy
  • Thyroid disease
  • Liver disease
  • Renal Disease
  • Thrombophilia
  • VTE
  • Obesity
  • Psychiatric
  • Reacreational Drug use
  • Anaemia
  • Haemoglobinopathies
  • Foetal Genital mutilation
197
Q

What types of diabetes are seen in pregnancy

A
  • Pre-existing
    • Type I
    • Type II
  • Gestational diabetes
198
Q

Define gestational diabetes

A
  • Carbohydrate intolerance which is diagnosed in pregnancy and may or may not resolve after pregnancy (NICE 2015)
  • Becoming more prevalent due toobesity and varying diagnostic thresholds
  • Pregnancy is a pro-diabetic state, therefore women with impaired glucose tolerance can deteriorate and be classified as diabetic in pregnancy
199
Q

How does NICE define gestational diabetes mellitues (GDM)

A
  • Fasting glucose ≥ 5.6 mmol/L OR
  • >7.8 mmol 2 hours after a 75g glucose load (Glucose tolerance test GTT)
200
Q

What are some feotal complications of GDM?

A

Complications due to elevated glucose levels

  • Cognenital abnormalities (NTD and cardiac) 3-4x
  • Preterm labour
    • Immature lungs compared to non-DM pregnancies
  • Macrosomia
  • Polyhydramnios
    • Polyuria, increased liqour
  • Dystocia and birth trauma
  • Foetal compromise, distress and sudden foetal death
    • Poor third trimester glucose control
201
Q

What are some maternal complications of GDM

A

Complications are related to glucose levels, so women with GDM (and better control) are less affected

  • Increased insulin requirements (300%)
    • Hypoglycaemias
    • Ketoacidosis (rare)
  • Infection
    • UTI
    • delivery wound or endometrial infection
  • Hypertension
  • Pre-eclampsia
  • Caeserean or instrumental delivery
    • Foetal compromise and macrosomia
  • Diabetic nephropathy
    • Proteinuria and renal deterioration
  • Diabetic retinopathy
    • Due to rapid control of blood glucose
202
Q

In a woman with pre-existing diabetes, what pre-conceptual care needs to be considered

A
  • Glucose control
    • Monthly HbA1c <6.5%
    • Preganancy not adviced it >10%
  • Fasting glucose 4-7 mmol/L
    • Metformin and insulin are appropriate, stop other hypoglycaemic drugs
  • Other
    • 5mg Folic acid
    • Stop statins
    • Switch to pregnancy safe anti-HTN (labeteolol, methyldopa)
    • Renal function; creatinine < 120 umol/L
    • Blood pressure
    • Retina assessment
203
Q

How do you monitor diabetes in preghnancy (when to test and test result aims)

A
  • HbA1c checked at booking
  • Glucose checked at home:
    • Fasted in the morning
    • Before meals
    • 1 hour after meals
    • Bedtime
  • Result aims: without hypoglycaemia
    • Fasting < 5.3 mmol/L AND
    • 1hour glucose < 7.8 mmol/L
  • Contact with healthcare professional should be no less than 2 weekly

  • NICE GDM =*
  • Fasting glucose ≥ 5.6 mmol/L OR*
  • >7.8 mmol 2 hours after a 75g glucose load (Glucose tolerance test GTT)*
204
Q

What are ttreatment options for glucose control for diabetes in pregnancy

A
  • Metformin OR Insulin
    • MEtformin dose will usually need to be increased as pregnancy advances and may need to be supplemented with insulin in type II
    • Insulin: combo of :
      • once or twice daily long-intermmediate acting AND 3 preprandial short-acting insulin injuections
    • Insulin pumps for poor control
    • Advise exercise and diet!
205
Q

In addition to the usual pregnancy scans, fetal echocardiography is indicated. Ultrasound is used to monitor _____ _____ and _____ _____ at _____ and _____ weeks. Even where glucose control has been good, macrosomia and polyhydramnios can occur (Fig. 21.5). Umbilical artery Doppler is not useful unless pre-eclampsia or intrauterine growth restriction (IUGR) develops.

A

In addition to the usual pregnancy scans, fetal echocardiography is indicated. Ultrasound is used to monitor fetal growth and liquor volume at 32 and 36 weeks. Even where glucose control has been good, macrosomia and polyhydramnios can occur (Fig. 21.5). Umbilical artery Doppler is not useful unless pre-eclampsia or intrauterine growth restriction (IUGR) develops.

206
Q

When is delivery advised in pregnancy with diabetes and what mode of delivery is recommended

A
  • Delivery 37-39 weeks
  • Elective C-section
    • Likely birth trauma if US (though unprecise) estimates fetal weight > 4kg
207
Q

What is used to control glucose levels during labour

A

Sliding scale of insulin and dextrose infusion

208
Q

What is the management overview/aim for diabetes in pregnancy

A
  • Preconceptual glucose control
  • Assess maternal diabetic complications
  • PAtient education and MDT]
  • Glucose monitoring and insulin adjustment
  • Anomaly and cardiac USS and foetal surveillance
  • Delivery 37-39 weeks
209
Q

How is GDM screened for

A

Risk-based screening; if +1 risk factors

  • Oral Glucose Tolerance Test (OGTT) at 24-28 weeks OR
  • If previous GDM, OGTT at 16-18 weeks. If normal repeat OGTT at 24-28 weeks
210
Q

What are some risk factors for GDM

A
  • Previous large baby (>4.5 kg) or Unexplained still birth
  • Previous history of GDM
  • First-degree relative (parents or siblings) with diabetes
  • BMI > 30
  • Minority ethnicity (S. asian, black Caribbean, Middle Eastyern)
  • Polyhydramnios
211
Q

What OGTT results would diagfnose GDM and therefore requires treatment

A
  • Fasting > 5.6 mmol/L OR
  • 2h glucose > 7.8 mmol/L
212
Q

What is the general management/overview of GDM

A
  • Explain Implications of GDM to mother and foetus
  • Blood glucose monitoring
  • Diet and exercise
  • Pharmacological management of glucose
213
Q

Outline the pharmacological management of gestational diabetes

A
214
Q

What AED are safe to use in pregnancy

A
  • Carbamezapine
  • Lamotrigine
215
Q

As well as switching to appropriate AEDs, what else needs to be done to manage epilepsy in pregnancy

A
  • 5mg Folic acid throughout pregnancy
  • 10mg Vit K po from 36 weeks
  • 20 week scan and feotal echocardiography to exclude foetal abnormalities
216
Q

What are maternal risks associated with obesity in pregnancy

A
  • Thromboembolism
  • Pre eclampsia
  • Diabetes
  • C-section
  • Wound infections
  • Difficult surgery
  • Postpartum haemorrhage
  • Maternal death
217
Q

What are foetal risks associated with obesity in pregnancy

A
  • Congenital abnormalities (NTD)
  • Diabetes
  • Perinatal mortality (pre-eclampsia)
218
Q

How is obesity managed in pregnancy

A
  • Preconceptual weight loss
  • Preconceptual 5mg Folic acid + Vitmain D
  • Weight is best maintained during pregnancy
    • Loss may lead to malnutrition
  • BMI > 35 = high risk pregnancy
  • BMI > 40 = formal anaesthetic risk assessment and antenatal thromboprophylaxis
219
Q

What are the two types of PROM

A
  • Premature rupture of membranes (PROM)
  • Pre-term premature rupture of membranes (PPROM)
220
Q

Define PROM

A
  • Rupture of foetal membranes at least 1 hour prior to onset of labour at ≥37 weeks gestation
  • 10-15% term pregnancies, minimal risk to mother and foetus due to advanced gestation
221
Q

Define PPROM

A
  • Rupture of foetal membranes occuring at <37 weeks gestation
  • Complicates 2% pregnancies and has high rate of maternal and foetal complications
  • Associated with 40% preterm deliveries
222
Q

Aetiology and pathophysiology or PROM/PPROM

  • The fetal membranes consist of the _____ and the _____. They are strengthened by _____, and under normal circumstances, become weaker at term in preparation for labour.
  • The physiological processes underlying this weakening include apoptosis and collagen breakdown by _____.
  • In cases of premature rupture of membranes and P-PROM, a combination of factors can lead to the early weakening and rupture of fetal membranes:
  • _____ – higher than normal levels of apoptotic markers and MMPs in the amniotic fluid.
  • _____ – inflammatory markers e.g. cytokines contribute to the weakening of fetal membranes. Approximately 1/3 of women with P-PROM have positive amniotic fluid cultures.
  • _____ _____
A
  • The fetal membranes consist of the chorion and the amnion. They are strengthened by collagen, and under normal circumstances, become weaker at term in preparation for labour.
  • The physiological processes underlying this weakening include apoptosis and collagen breakdown by enzymes.
  • In cases of premature rupture of membranes and P-PROM, a combination of factors can lead to the early weakening and rupture of fetal membranes:
    • Early activation of normal physiological processes – higher than normal levels of apoptotic markers and MMPs in the amniotic fluid.
    • Infection – inflammatory markers e.g. cytokines contribute to the weakening of fetal membranes. Approximately 1/3 of women with P-PROM have positive amniotic fluid cultures.
    • Genetic predisposition
223
Q

What are some risk factors for PROM/PPROM

A
  • Smoking (esp <28 wk gest)
  • Previous PROM/pre-term delivery
  • Vaginal bleeding during pregnancy
  • Lower genital tract infecition
  • Iatrogenic (amniocentesis)
  • Polyhydramnios
  • Multiplpe pregnancy
  • Cervical insufficiency

In many cases of PROM/PPROM, there are no identifiable risk factors

224
Q

What are some clinical features of PROMS

A
  • Typical history of broken water
    • Painless popping senstion followed by gush of watery fluid from the vagina
  • Can be non-specific - gradual leak
  • Speculum - may see pooling in posterior vaginal fornix
    • Speculum not needed if amniotic fluid is seen draining from vagina
  • Lack of normal vaginal discharge (washed clean)
225
Q

Differential diagnosis for PROMS

A
  • Urinary incontinence
  • Normal vaginal secretions in pregnancy
  • Cervical infection
  • Loss of mucus plug
226
Q

What are some investigations for PROMs/PPROMs

A

Diagnosis usually made by i) maternal history of membrane rupture and ii) positive examination findigns

  • High vaginal swab in ALL cases
    • May grow GBS, which would indicate intrapartum Abx
  • ferning test
    • Leting cervical secretions dry from a glass slide - forms fern-pattern
  • Ultra sound
    • Not routinely used but can be used if diagnosis unclear
      *
227
Q

With regards to management of PROMs, what factors are considered to guide management

A
  • Rupture of membrane will stimulate uterus - therefore majority of women go into labour withing 24-48 hours
  • If women do not go into labour, induction of labour may be considered:
    • Balancing gestational age (dont induce so foetus can develop more)
    • Risk of infection

Summary: IOL and delivery if >34 weeks

Expectant management if < 34 weeks

228
Q

What is the management of PROM if it occure >36 weeks gestation

A

Expectant management

  • wait 24hr as 60% go into labour naturally
  • IOL recommended if >24hr
  • Monitor signs of clinical chorioamnionitis
  • High vaginal swab
    • Clindamycin/penicillin intrapartum if +ve
229
Q

What is the management of PROM if it occure 34-36 weeks gestation

A
  • IOL and delivery recommended
  • Monitor signs of chorioamnionitis
    • Avoid sexual intercourse
    • Prophylactic erythromycin 250mg QDS for 10 days
  • high vaginal swab
    • Clindamycin/penicillin intrapartum
  • Corticosteroids
230
Q

What is the management of PROM if it occure 24-33 weeks gestation

A
  • Aim expectant management until 34 weeks
  • Monitor signs of chorioaminonitis
    • Avoid sexual intercourse
    • Prophylactic erythromycin 250mg QDS 10days
  • Corticosteroids

Historically the aim was to get the pregnancy to 36 weeks if there was no evidence of infection. However, with improvements in neonatal care (and evidence for poorer outcomes in babies if there is maternal infection), management has shifted towards 34 weeks and induction of labour once there has been a course of steroids.

231
Q

Complications of PROM

A

Outcome or PROM correlates with gestational age of foetus. Majority women go into labour after PROM but there is a greater latency period the younger the gestational age. Pre-disposes greater risk of maternal and foetal complications

  • Chorioamnionitis
    • Infection of foetal membrane
    • Risk increases longer membranes remained ruptured and baby undelivered
  • Oligohydramnios
    • Sig in <24 weeks gestation, increases risk of lung hypoplasia
  • Neonatal death
    • Prematurity, sepsis, pulmonary hypoplasia
  • Placental abruption
  • Umbilical cord prolapse
232
Q

Define induction of labour (IOL)

A
  • Process of starting labour artificially
  • Most women go into labour sponataneously by 42 weeks of gestation, roughly 1 in 5 will require an induction
  • IOL performed when its though that the baby will be safer delivered than remaining in utero. Also could be due to concerns for maternal health
233
Q

What is the general indication for IOL and name 5 specific contexts where IOL is indicated

A

IOL indicated when delivering baby is safer for the baby and or mother thanfor baby to remain in utero

  • Prolonged gestation
  • PROM/PPROM
  • Maternal health problems
  • Foetal growth restriction
  • Intrauterine foetal death
234
Q

In women with prolonged gestation, when should they be offered IOL

A
  • If uncomplicated, offer between 41+0 to 42+0 weeks’ gestation.
235
Q

In women with prolonged gestation, what is the aim of IOL

A
  • Avoid risk of foetal compromise and still birht (thought to be secondary to placental ageing)
236
Q

If a patient with prolonged gestation declines an IOL, how should she be managed

A
  • Increased frequency of monitoring from 42 weeksa onwards
  • at least twice‑weekly cardiotocography and ultrasound estimation of maximum amniotic pool depth
237
Q

What is the management of PROM in terms of delivery

A

>37 week gestation

  • Offer IOL
  • OR expectant management for a maximum 24 hours
    • Any longer increases risk of ascending infection -chorioamnionitis
    • 84% women will spontaneously go into labour withitn first 24 hours
  • High vaginal swab
  • Clindamycin/penicillin intrapartum if +ve
238
Q

What is the management of P-PROM in terms of delivery

A

Dependent on stage of gestation:

<34 weeks gestation

  • Delay IOL unless obstetric factors indicate otherwise (foetal distress) - Aim for 34 weeks gestation
  • Monitor signs of chorioaminonitis
    • Avoid sexual intercourse
    • Prophylactic erythromycin 250mg QDS 10days
  • Corticosteroids

>34 weeks gestation

  • IOL and delivery recommended
    • Timing depends on risk v benefits of delaying pregnancy further (increased risk of infection)
  • Monitor signs of chorioamnionitis
    • Avoid sexual intercourse
    • Prophylactic erythromycin 250mg QDS for 10 days
  • high vaginal swab
    • Clindamycin/penicillin intrapartum
  • Corticosteroids
239
Q

What are some examples of maternal health problems which would indicate IOL

A
  • Hypertension
  • Pre-eclampsia
  • Diabetes
  • Obstetric Cholestasis

Decision will depend on health of mother and foetus

240
Q

What is the second most common indication for IOL and what is the aim of IOL in this context

A
  • Foetal growth restriction
  • Aim: Deliver baby prior to foetal compromise
241
Q

When can you offer IOL in a woman with intrauterine foetal death

A
  • MOther physically well with intat membranes
242
Q

What are some absolute contraindications for IOL

A
  • Ceophalopelvic disproportion
  • Major placenta praevia
  • Vasa praevia
  • Cord prolapse
  • Transverse lie
  • Active primary genital herpes
  • Previous classical C-Section
243
Q

What are some relative contraindications to IOL

A
  • Breech presentation
  • Triplet or higher order pregnancy
  • Two or more previous low transverse C-section
244
Q

What does IOL increase the risk of with a women who has had a previous c-section

A

Increased risk of:

  • Emergency caeseran
  • Uterine rupture
245
Q

What are the three types of breech presentation

A
  • Frank breech
  • Complete breech
  • Incomplete breech
    • Footling breech
    • Kneeling breech
246
Q

What are the three main methods of induction

A
  • Vaginal prostaglandins
  • Amniotomy
  • Membrane Sweep
247
Q

What is the mainstay method of IOL (1st line NICE 2008) and describe how it works

A
  • Vaginal prostaglandins
  • Prostaglandins
    • act to prepare the cervix by ripening it
    • have a role in contraction of smooth muscle of uterus
248
Q

What are the two regimens for vaginal prostaglandin induction and describe how they are taken/differences

A
  • Tablet/gel regimen
    • 1 cycle = 1st dose, plus 2nd dose if labour has not started within 6 hours
  • Pessary regimen
    • 1 cycle = 1 dose over 24 hours

Recommended maximum of one cycle in 24 hours (IOL can sometimes take multiple days)

249
Q

Describe how amniotomy can be used in IOL

A
  • Membranes are ruptured artificially using an amniohook
  • Like in membrane sweep, this process releases prostaglandins in an attempt to expedite labour
  • Often given with Syntocinon infusion
250
Q

How does a Syntocinon infusion help in amniotomy?

The aim is to start _____ and titrate _____ until there are _____ (number) _____ every _____ minutes

A
  • Increases strength and frequemncey of contractions

The aim is to start low and titrate upwards until there are 4 contractions every 10 minutes

251
Q

The aim of amniotomy + syntocinon infusion is to start _____ and titrate _____ until there are _____ (number) _____ every _____ minutes

A

The aim of amniotomy + syntocinon infusion is to start low and titrate upwards until there are 4 contractions every 10 minutes

252
Q

What is the indication for amniotomy +/- syntocinon

A
  • NOT FIRST LINE for IOL
  • Only when cervis is ripe (Bishop Score ≥ 7)
  • OR Prostaglandin use is contraindicated (high risk of uterine hyperstimulation)
253
Q

Describe the process involved in membrane sweep and how it helps in IOL

A
  • Inserting gloved finger through cervix and rotating against foetal membranes
  • Aims to separate chorionic membrane from the decidua
  • Separation helps release natural prostaglandins to attemtp to kick-start labour
254
Q

When would you offer membrane sweep for IOL

A

Used as an adjunct of IOL. Perfomring it increases likelihood of spontaneous delivery reducing need for formal induction

  • 40-41 weeks nulliparous women
  • At 41 weeks multiparous women
255
Q

How is IOL monitored

A
  • Bishop Score
  • CTG
256
Q

What does the Bishop score measure

A
  • Assessment of cervical ripeness based on factors taken during vaginal examination
  • Checked prior to induction and during induction to assess progress (6 hours post-tablet/gel, 24 hours post-pessary)
257
Q

What are the factors that make up Bishop Scoring

A
  • Dilation (cm) of cervix
  • Length of cervix (cm)
  • Station (relative to ischeal spines)
  • Consistency of cervix
  • Position of cervix
258
Q

What are the scoring thresholds for the Bishop Score

A
  • ≥ 7 = cervix is ripe or favourable
    • High cance of responsiveness to interventions made to induce labour (ie IOL possible)
  • <4
    • Labour unlikely to progress naturally
    • therefore prostaglandin therpay required
259
Q

If the cervix fails to ripen despite prostaglandin use, what may you need to consider

A

Caeserian section

260
Q

When and what things should you be looking out for on CTG during IOL

A
  • CTG prior to IOL to confirm reassuring foetal HR
  • After IOL initiation, when contraction begins, assess foetal HR until normal rate is confirmed (use continuous CTG)
    • Subsequently assess using intermittent auscultation
  • If oxytocin infusion is stated, mointor using continuous CTG throughout labour
261
Q

Complications of IOL and briefly describe how you would manage them

A
  • Failure of induction (15%)
    • Offer further cycle of prostaglandins or C-section
  • Uterine hyperstimulation (1-5)
    • Contractions too long or too frequent leading to foetal distress
    • Manage with tocolytics (terbutaline)
  • Cord prolapse
    • Can occur at amniotomy, esp when presentation of foetal head is high
  • Infection
    • Fewer veginal examinations
  • Pain
    • IOL more painful than spontaneous labour
    • Epidural analgesia
  • Uterine rupture (rare)
  • Increased rate of further intervention vs spontaneous labour
262
Q

Define caeserian section

A

Delivery of baby through surgical incision in the abdomen and uterus

263
Q

What are the classifications of caeserian section

A
  • Category 1
    • Immediate threat to life of woman or foetus
    • Deliver in 30 minutes (some 20 min)
  • Category 2
    • Maternal or foetal compromise that is not immediately life-threatening
    • Deliver in 60-75 minutes
  • category 3
    • No maternal or foetal compromise but needs early delivery
  • Category 4
    • Elective
264
Q

What are the two most common reasons for an emergency C0-section

A
  • Failure to progress in labour
  • Suspected/confirmed foetal compromise
265
Q

What are some indications for an elective C-section

A
  • Breech presentation at term
  • Other malpresentations
    • Unstable, Transverse, Oblique lie
  • Twin pregnancy
    • When first twin is NOT cephalic presentation
  • Maternal medical conditions
    • Cardiomyopathy
  • Foetal compromise
  • Transmissable disease
    • Poorly controlled HIV
  • Primary genital herpes
    • in third trimester
  • Placenta praevia
  • Maternal diabetes
    • Foetal weight > 4.5 kg
  • Previous major shoulder dystocia
  • Previous 3rd/4th perineal tear
  • Maternal request
266
Q

At what gestational week are elective C-sections planned for and why is this

A
  • After 39 weeks
    • Reduce respiratory distress in neonate (TTN)
  • If before 39 weeks consider corticosteroid administration
    • Developmoent of foetal lungs
267
Q

What are some pre-operative investigations and management for elective C-section

A
  • FBC and G&S
    • blood loss 500-1000mL
  • H2-receptor antagonist
    • Ranitidine +/- ?metoclopramide
  • VTE risk score
    • TED stockings +/- LMWH
  • Type of anaesthesia
    • Regional anaesthetis (epidural or spinal)
    • General anaesthetic
268
Q

What is Mendelson’s Syndrome

A
  • Aspiration of gastric contents into the lung leading to chemical pneumonitis
  • Caused by pressure from gravid uterus on gastric ocntents
269
Q

Layers the needle goes through for a spinal anaesthesia

A
  • Skin
  • Fat
  • Muscle
  • Suprspinous ligaments
  • Interspinous ligaments
  • Ligamentum flavum
  • Dura
  • Subdural space
  • Arachnoid mater
  • Subarachnoid space
270
Q

Roughly outline the operative procedure in C-setions

A
  • Pre-incision
    • Left lateral tilt of 150 - reduce risk of supine hypotension due to aortocaval compression
    • Foley’s catheter - drain bladder and reduce risk of injury
    • Skin cleaned and antibiotics administered
  • Skin incision
  • Sharp or blunt dissection into abdomen
  • Incision of visceral peritoneum
  • Uterine incision
  • Oxytocin 5IU
  • Closure
271
Q

Name two types of transverse lower abdominal skin incisions for c-sections

A
  • Pfannenstiel
  • Joel-Cohen
272
Q

Compare and contrast transverse low incisions and midline incisions for c-section

A
273
Q

What are the layers of the abdomen that are cut through during shapr/blunt dissection

A
  • Skin
  • Camper’s fascia - superficial layer of SC tissue
  • Scarpa’s fascia - deep membranous layer of SC tissue
  • Rectus sheath - anterior and posterior
  • rectus muscle
  • Parietal peritoneum (abdominal)
  • Uterus/bladder
274
Q

When reaching the visceral peritoneum, what is used to retract the bladder

A

Doyen retractor

275
Q

What types of uterine incisions are used in c-section

A
  • Transverse curvilinear incision
    • Digitally extended
  • De Lee’s incision
    • Lower vertical - required if lower uterine incision is poorl;y formed(rare
276
Q

Why is oxytocin given once baby delivered by c-section

A
  • given IV by anaesthetist to aid delivery of placenta by controlled cord traction by surgeon
277
Q

What observations are measured post-operatively c-section

A
  • Early warning chart
  • Lochia
    • PV bleed loss
278
Q

What are encouraged pos-c section to enhance recovery

A

Early mobilisation

Eating and drinking

removal of catheter

279
Q

A primary c-section reduces the risk of what

A
  • Perineal trauma and pain
  • Urinary incontinence
  • Anal incontinence
  • Uterovaginal prolapse
  • Late stillbirth
  • Early neonatal infection
280
Q

What are some immediate complications of c-section

A
  • PPH >1000mL
  • Wound haematoma (high BMI, diabetes, immunosup.)
  • Intra-abdo haemorrhage
  • Bladder/bowel trauma (esp in those with previous abdo surgery)
  • Neonatal
    • TTN
    • Foetal lacerations
281
Q

What are some intermediate complications of c-section

A
  • Infection
    • UTI
    • Endometritis
    • Respiratory (in GA)
  • VTE
282
Q

What are some late complications of C-section

A
  • Urinary tract trauma (fistula)
  • Subfertility
  • Psyhcological sequelae
  • VBAC - Vaginal birth after c-section
  • Placenta Praevia/accrete
  • Caeserean scar ectopic pregnancy
283
Q

What are the two delivery options in a patient with previous C-section

A
  • Vaginal birth after C-section (VBAC)
  • Planned elective repeat C-section
284
Q

VBAC is clinically safe for the majority of women who have had one prior lower segment c-section (NICE, RCOG, ACOG). More complex circumstances requires caution and senior obstetrician care. What are some examples of these complex circumstances

A
  • Multiple pregnancy
  • Macrosomia
  • Maternal age > 40 y
285
Q

For each of the following, identify whether each one is referring to VBAC or elective repeat C-Section (ERCS)

  • Shorter hospital stay and recovery
  • Greater risk of uterine rupture
  • No risk of anal sphincter injury
  • Higher risk of maternal death
  • Likely to require future C-Section
  • Higher risk of neonatal respiratory morbidity
  • Higher risk of hypoxic ischaemic encephalopathy (HIE)
  • Increased risk of placental problems and adhesion formation
A
  • Shorter hospital stay and recovery - VBAC
  • Greater risk of uterine rupture - VBAC
  • No risk of anal sphincter injury - ERCS
  • Higher risk of maternal death - ERCS
  • Likely to require future C-Section - ERCS
  • Higher risk of neonatal respiratory morbidity - ERCS
  • Higher risk of hypoxic ischaemic encephalopathy (HIE) - VBAC
  • Increased risk of placental problems and adhesion formation - ERCS
286
Q

What are some considerations/management of VBAC

A
  • Deliver in hospital setting (emergency c-section and advanced neonatal resuscitation)
  • Continuous CTG monitoring
  • Additional analgesic requirements
  • Avoid induction where possible
    • risk of rupture is less with mechanical tehcniques (amniotomy) vs with prostaglandins
  • Augmentation can increase risk of uterine scar rupture
  • Senior obstetrician input
  • >39 weeks = recommended elective repeat C-section
    *
287
Q

What are the absolute contraindications to VBAC

A
  • Classical caeserean scar
  • Previous uterine rupture
  • Other contraindications for vaginal birth that apply to the clinical scenario (eg placenta praevia)
288
Q

What are the relative contraindications for VBAC

Made on case-by-case basis by senior obstetrician

A
  • Complex uterine scars
  • >2 prior lower segment C-sections
289
Q

Define uterine rupture

A
  • Full thickness disruption of uterine muscle and overlying serosa
  • Foetus can be extruded from uterus resulting in foetal hypoxia and large internal haemorrhage

RARE but significant maternal and foeatl morbidity nad mortality

290
Q

Describe the two types of uterine rupture

A
  • Incomplete
    • Peritoneum overlying uterus is intact
    • Uterine contents remain in the uterus
  • Complete
    • Peritoneum is also torn
    • Uterine contants can escape into the petioneal cavity
291
Q

What are the risk factors of uterine rupture

A
  • Previous C-section
  • Previous uterine surgery (myomectomy)
  • Induction (prostaglandins or augmentation of labour)
  • Obstruction of labour
    • Developing countries
  • Multiple pregnancy
  • Multiparity
292
Q

Clinical features (symptoms) of uterine rupture

A

Non-specific

  • Abdominal pain
    • Persists between contractions
  • Shoulder tip pain
  • Vaginal bleeding
293
Q

Signs of uterine rupture (on examination)

A
  • Regression of presenting part
  • Scar tenderness on palpation
  • Palpable foetal parts
  • Hypovolaemic shock
    • Significant haemorrhage
  • Foetal distress or absent heart sounds
294
Q

Differentials for uterine rupture

A
  • Placental abruption
    • Abdo pain +/- vaginal bleeding
    • Uterus often described as tense on palpation and woody
  • Placenta praevia
    • Painless vaginal bleeding
  • Vasa praevia
    • Triad:
      • Ruptured membranes
      • Painless vaginal bleeding
      • Foetal bradycardia
295
Q

Vasa praevia triad

A
  • Painless vaginal bleeding
  • Rupture of membranes
  • Foetal bradycardia
296
Q

Investigations for uterine rupture

A
  • Intrapartum CTG (in women at risk of rupture)
    • Recurrent or late decelerations
    • Proloinged foetal bradycardia
  • Maternal haematuria
    • Catheter
  • Ultrasound
    • Suspicion of uterine rupture in pre-labour setting
    • Abnormal foetal lie or presentation
    • Haemoperitoneum
    • Abesnt uterine wall
297
Q

Management of uterine rupture

A

OBSTETRIC EMERGENCY

  • Call for senior help and appropriate staff
  • A-E approach
  • 222 call
  • Resuscitation
  • Surgical management
298
Q

Surgical management of uterine rupture

A
  • Deliver by C-section
  • Uterus repair or hysterectomy
  • Decision-incision interval in operative intervention should be <30 minutes
299
Q

Define operative vaginal delivery (OVD)

A

Use of an instrument to aid delivery of foetus

300
Q

What are the two instrument types used in operative deliveries

A
  • Ventouse
  • Forceps
301
Q

Which of the two instruments used in OVDs tend to have a lower risk of ofetal complications and higher risk of maternal complicatiosn

A
  • Forcep delivery
302
Q

When using instruments in an OVD, when should the attempt be abandoned

A
  • Abandon if after three contractions and pulls with any instrument, there is no reasonable progress
303
Q

What are some ventouse types

A
  • Silastic cup attached to electric pump
    • Only if foetus in occipital-anterior position
  • Kiwi - handheld disposable device
    • Omni-cup, used for all foetal positions and rotational deliveries
  • Bird cup
    • Occipital-posterior positions
304
Q

Where should the cup in ventouse be placed

A
  • Cup with centre over the flexion point of the foetal skull
    • Midline, 3cm anterior to the posterior fontanelle

During contractions, traction is applied perpendicular to the cup

305
Q

Ventouse deliveries are associated with:

  • Lower/higher success rate
  • Less/more maternal perineal injuries
  • Less/more pain
  • Less/more cephalhaematoma
  • Less/more Subgaleal haematoma
  • Less/more foetal retinal haemorrhage
A
  • Lower success rate
  • Less maternal perineal injuries
  • Less pain
  • More cephalhaematoma
  • More Subgaleal haematoma
  • More foetal retinal haemorrhage
306
Q

Forceps are double bladed instruments. Name some different types

A
  • Rhodes, Neville-Barnes or Simpsons
    • OA positions
  • Wrigley’s
    • C-section
  • Kielland’s
    • Rotational deliveries
307
Q

How are forceps used in OVD

A
  • Blades introduced to pelvis (taking care not to cause trauma to maternal tissue)
  • Applied around sides of foetal head
  • Blades lock together
  • Gentle traction during uterine contractions, following the J shape of the maternal pelvis
308
Q

Use of forceps is associated with:

  • Lower/Higher rate of 3rd/4th degree tears
  • Used less/more often to rotate
  • Requires/Does not require maternal effort
A
  • Higher rate of 3rd/4th degree tears
  • Used less often to rotate
  • Does not require maternal effort
309
Q

Indications of OVD

A

Considered in 2nd stage of labour. Is there a valid clinical indication to intervene? Is the patient a suitable case for an intrumental delivery?

Maternal:

  • Inadequate progress
    • Nulliparous women - general rule to expect delivery after two hours of active pushing
    • Multiparous women - expect delivery within one hour of active pushing
  • Maternal exhaustion
  • Maternal medical conditions that means active pushing or prolonged exertions should be avoidied
    • Intracranial patholgies
    • Maternal congenital heart disease
    • Severe hypertension

Foetal

  • Suspected foetal compromise in 2nd stage of labour
    • CTG monitoring
    • Abnormal foetal blood sample
  • Clinical concerns
    • Significant antepartum haemorrhage
310
Q

What are some pre-requisites for instrumental delivery

A
  • Fully dilated
  • Ruptured membranes
  • Cephalic presentation
  • Defined foetal position
  • Foetal head at least at the level of ischial spines and no more than 1/5 palpable per abdomen
  • Empty bladder
  • Adequate pain relief
  • adequate maternal pelvis
311
Q

What are the absolute contraindications of OVD

A
  • Unengaged foetal head in singletone pregnancies
  • Incompletely dilated cervix in singleton pregnancies
  • True cephalo-pelvic disproportion (foetal head too large to pass through maternal pelvis)
  • Breech and face presentation
  • Preterm gestation (<34 weeks) for ventouse
  • High likelihood of fetal coagulation disorder for ventouse
312
Q

What are some relative contraindications to OVD

A
  • Severe non-reassuring foetal status, with station of the head above the level of pelvic floor (foetal scalp not visible)
  • Delivery of second twin when the head is not quite engaged or the cervix has reformed
  • Prolapse of the umbilical cord with foetal compromise when the cervix is completely dilated and the station is mid cavity
313
Q

How is OVD classified (no descriptiuon)

A

Classified by degree of foetal descent. The lower the classification, the less the risk of complications

314
Q

Describe the three classifications of OVD

A

Outlet

  • Foetal scalp visible with labie parted
  • Foetal skull reached pelvic floor
  • Foetal head on perineum

Low

  • Lowest presenting part (not caput) is +2, or further below the ischial spines. subdivided to:
    • >45 degrees - rotation needed
    • <45 degrees - no rotation needed

Midline

  • 1/5 palpable abdominally. Lowest part is above +2 but is lower than ischial spines. Subdivided to:
    • >45 degrees - rotation needed
    • <45 degrees - no rotation needed
315
Q

Complications of OVD

A

Foetal

  • Neonatatl jaundice
  • Scalp lacerations
  • Cephalhaematoma
  • Subgaleal haematoma
  • Facial bruising
  • Facial nerve damage
  • Skull fractures
  • Retinal haemorrhage

Maternal

  • Vaginal tears (3rd/4th degree)
    • Forceps >> ventouse > vaginal delivery
  • VTE
  • Incontinence
  • PPH
  • Shoulder dystocia
  • Infection
316
Q

Define small for gestational age (SGA)

A
  • Infant birth weight <10th centile for gestational age
  • Severe SGA = birth weight <3rd centile
317
Q

Define foteal small for gestational age

A
  • Estimated foetal weight (EFW) or adbominal circumference (AC) <10th centile
  • Severe = EFW or AC < 3rd centile
318
Q

Define foetal growth restriction (FGR)

A
  • When genetic growth is restricted by a pathological process
  • This can present with features of foetal compromise:
    • Reduced liqour volume
    • Abnormal doppler studies
  • Likelihood of FGR is higher in severe SGA foetus
319
Q

Define the boundary of a low birth weight

A
  • Birth weight <2.5kg (2500g)
320
Q

What are the 3 aetiologies/pathophysiologies of a small for gestational age baby

A
  • Normal (constitutionally) small
  • Placenta mediated growth restriction
  • Non-placenta mediated growth restriction
321
Q

Describe what is meant by a normal (constitutionally) small baby

A
  • Small size at all stages but follows growth centiles
  • No pathology is present
  • Conrtibuting factors include ethnicity, sex, parental height

50-70% SGA foetus/infants are consitutionally small

322
Q

Describe the pathophysiology of placenta mediated growth restriction

A
  • Growth normal initially but slows in utero
  • Leads to placental insufficiency
  • Common cause of FGR and can be due to maternal factors
323
Q

Describe some maternal factors that can lead to placenta-mediated growth restriction (placental insufficiency)

A
  • Low-pregnancy weight
  • Substance abuse
  • Autoimmune disease
  • Renal disease
  • Diabetes
  • Chronic HTN
324
Q

Describe the pathophysiology under non-placenta mediated growth restriction

A
  • Growth affected by foetal factors
    • Chromosomal or structural anomaly
    • Error in metabolism
    • Foetal infection
325
Q

When are women assessed for risk factors of SGA

A
  • Booking visit AND
  • 20 weeks gestation
326
Q

What are some minor risk factors for SGA

A
  • Maternal age ≥35
  • Smoker 1-10/day
  • Nulliparity
  • BMI < 20 or 25-34.9
  • IVF singleton
  • Previous pre-eclampsia
  • Pregnancy interval <6 or ≥60 months (5 years)
  • Low fruit-intake pre-pregnancy
327
Q

What are some major risk factors for SGA

A
  • Maternal age >40
  • Smoker ≥ 11/day
  • Previous SGA baby
  • Maternal/paternal SGA
  • Previous stillbirth
  • Cocaine use
  • Daily vigorous exercise
  • MAternal disease (Chronic HTN, renal impariment, diabetes w/ vascular disease, APS)
  • Heavy bleeding
  • Low PAPP-A
328
Q

When would you refer someone for UAD surveillance in SGA

A
  • 3 minor risk factors present -> UAD
  • Major risk factor present -> serial ultrasound and UAD
329
Q

How is SGA investigated/diagnosed

A
  • Ultrasound
    • Diagnosis and surveillance of SGA
  • Foetal anatomical survey
  • Uterine artery doppler (UAD)
  • Karyotyping
  • Infection screen
    • Congenitcal CMV
    • Congenital toxoplasmosis
    • Congenital syphilis
    • Congenital malaria
330
Q

What features are you looking for on ultrasound scan for SGA

A
  • Biometrics - plotted on centil charts (take into account maternal height, weight, ethnicity, parity)
    • EFW (estimated foetal weight)
    • Abdominal circumference (AC)
  • Head circumferenc (HC):AC ratio
    • Symmetrically small foetus likely to be constitutionally small
    • Asymmetrically small foetus more likely due to placental insufficiency
    • Brain sparing effect
  • Reduced amniotic fluid
    • Impaired foetal kidney function as a result of placental insufficiency
331
Q

Overview of the management of SGA

A
  • Prevention
  • Surveillance
  • Delivery
332
Q

In the management of SGA, describe the details of prevention

A
  • MAnage modifieable risk factors for SGA
    • Smoking cessation
    • Optimise maternal disease
  • 75mgaspirin 16 weeks gestation until delivery
    • For women at high risk of pre-eclampsia
333
Q

In the management of SGA, describe surveillance

A
  • Uterine artery doppler (AUD) primary surveillance tool in SGA foetus
    • If normal, repeat every 14d
    • If abnormal, repeat more frequently and consider delivery
  • Other surveillance tests:
    • Symphysis fundal height (SFH)
    • Middle Cerebral artery (MCA) doppler
    • Ductus venous (DV) doppler
    • CTG
    • Amniotic fluid volume
334
Q

In the manfemetn of SGA, outline the features of devliery

A
  • If considering delivery 24 to 35+6 weeks gestation = single course antenatal steroids
335
Q

What is a maternal complciation of SGA

A

Increased risk of still-birth

336
Q

What are some neonatal complications of SGA

A
  • Birth asphyxia
  • Meconium aspiration
  • Hypothermia
  • Hypo/Hyperglycaemia
  • Polycythaemia
  • Retinopathy of prematurity
  • Persistent pulmonary hypertension
  • Pulmonary haemorrhage
  • Necrotising enterocolitis
337
Q

What are the long term neonatla complications of SGA

A
  • Cerebral palsy
  • T2DM
  • Obesity
  • Hypertension
  • Precocious puberty
  • Behavioural problems
  • Depression
  • Alzheimer’s disease
  • Cancer (breast, ovarian, colon, lung, blood)
338
Q

Define prolonged pregnancy

A
  • Pregnancies which persist up to and beyond 42 weeks gestation
  • AKA Post-term or post-dates pregnancy
  • 5-10% pregnancies
339
Q

What are some risk factors of prolonged pregnancies

A

Unlcear but:

  • Nulliparity
  • Maternal age >40
  • Previous prolonged pregnancy
  • High BMI
  • FH of prolonged pregnancies
340
Q

What are some clinical features of prolonged pregnancy

A
  • Static growth
  • Maybe macrosomia
  • Oligohydramnios
  • Reduced foetal movements
  • Presence of meconium
    • Meconium staining (on nails)
  • Dry/flaky skin with reduced vernix
    • Vernix is white, waxy substance on skin of newborn babies
341
Q

Investigations for prolonged pregnancy

A
  • Diagnosis based on gestational age
  • Dating between 11+0 and 13+6 weeks in first trimester is most reliable as foetus rarely shows signs of being consitutionally large or small until later gestational stage
  • Ultrasound scanning to check growth, liqour volume, dopplers performed in women with prolonged pregnancy
342
Q

Management of prolonged pregnancy

A

NICE/RCOG:

Deliver by 42 weeks gestation to reduce risk of stillbirth

  • Membrane sweep (offer from 40+0 in nulliparous and 41+0 in parous women)
  • IOL (offer 41+0 and 42+0)

Women who decline IOL should be offereed twice weekly CTG monitoring and USS with amniotic fluid measurement to identify foetal distress, in which case emergency c-section might be indicated

343
Q

complication of prolonged pregnancy

A
  • Increased risk of still birth
    • Rate exponentially rises after 37 weeks gestation
  • Foetal acidaemia and meconium aspiration in labour
    • Due to placental insufficiency
  • Neonatal hypoglycaemia
    • Placental degradataion/insufficiency, so reduced O2 and nutrient transfer
    • Can deplete foetal glycogen stores
344
Q

Define placental abruption

A
  • when part of or all of placenta separates from the wall of the uterus prematurely
  • Important cause of antepartum haemorrhage (pv bleed from week 24 until delivery)
345
Q

Describe the pathophysiology of placental abruption

A
  • Occus following a rupture of materna lvessels within basal layer of endometrium
  • Blood accumulates and splits the placental attachment form the basal layer
  • Detached portion of placenta is unable to function leading to foetal compromise
346
Q

What are the two types of placental abruption and describe themAttach Images

A
  • Revealed
    • Bleeding tracks down from the site of placental separation and drains through the cervix
    • Results in vaginal bleeding
  • Concealed
    • Bleeding remains in the uterus and typically forms a clot retroplacentally
    • Bleeding is not visible but can be severe enought to cause systemic shock
347
Q

Risk factors for placental abruption

A
  • Previous placental abruption (most predictive factor)
  • Pre-eclampsia and HTN disorders
  • Abnormal lie of baby (transverse)
  • Polyhydramnios
  • Abdominal trauma
  • Smoking or drug use (cocaine)
  • Bleeding in first trimester
    • Haematoma is seen inside uterus on first trimester scan
  • Underlying thrombophilias
  • Multiple pregnancy
348
Q

Clinical features of placental abruption

A
  • Painful vaginal bleeding
    • Bleedig may be concealed
    • Inquire about pain during contraction if in labour
  • O/E, uterus may be woody (tense all the time) and painful on palpation
349
Q

Differential diagnosis for antenatal haemorrhape

A
  • Placental abruption (not most common)
  • Placenta praevia
  • Marginal placental bleed
    • Small placental abruption large enough to cause revealed bleeding but small enough not to cause maternal or foetal compromise
  • Vasa praevia
  • Uterine rupture
  • Local genital cause
    • Benign or malignant
      • Polyps, carcinoma, cervical ectropion (common)
    • Infection
      • Candida, bacterial vaginosis, chlamydia
350
Q

Investigations for placental abrutpion

A
  • Haematology
    • FBC
    • Clotting profile
    • Kleihauer test
      • if woman is Rh negative, to determine amount of foeto-maternal haemorrhage and this the dose of Anti-D required
    • Group and save
    • Cross match
  • Biochemistry
    • U&E
    • LFT
    • exclude hypertensive disroders (pre-eclampsia, HELLP)
  • Foetal wellbeing - CTG
  • Imaging
    • Ultrasound scan
      • Whwen patient is stable
      • retroplacental haematoma might be seen
      • Good positive predictive value but poor negative predictive value
      • Therefore should not be used to exclude abruption
351
Q

Management of placental abruption

A
  • ABCDE approach

Ongoing management of placental abruption is dependent of foetal health

  • Emergency delivery
    • C-section if there is maternal or foetal compromise
  • IOL
    • Haemorrhage at term without maternal/foetal compromise
    • Recommende to avoid further bleeding
  • Conservative
    • Some partial or marginal abruptions without maternal or foetal compromise

All cases give anti-D within 72 hours on the onset of bleeding if woman is Rh -ve

352
Q

Describe the different types of multiple pregnancy

A
  • Dizygotic twins (DZ)
    • Results from fertilisation of different oocytes by different sperm
    • Foetuses can be different sexes and are no more genetically similar than siblings from different pregnancies
  • Monozygotic twins (MZ)
    • Results from mitotic division of a single zygote into identical twins.
    • Whether they share the same amnion or placenta depends on the time at which division into separate zygotes occured
353
Q

In monozygotic twins (MZ), what determines wherther they share the same placenta or same amnion

A

The time at which the zygote divides to form separate zygotes

354
Q

Describe the different types of placenta- / amnion- sharing seen in monozygotic twin pregnancies

A
  • Dichorionic diamniotic (DCDA)
    • Division before day 3
  • Monochorionic diamniotic (MCDA)
    • Division 4-8 day
  • Monochorionic monoamniotic (MCMA)
    • Division 9-13 days
  • Conjoined twins
    • Incomplete division

Placenta basically established earlier than amnion.

355
Q

_____ twins have a higher foetal loss rate, particularlty before _____ weeks

A

Monochorionic twins have a higher foetal loss rate, particularlty before 24 weeks

356
Q

What are some factors associated with multiple pregnancy

A
  • Increasing maternal age - DZ twinning
  • Increasing parity - DZ twinning
  • Assisted conception
    • 20% IVF conceptions
    • 5-10% clomiphene-assisted conceptions
  • Genetic factors
357
Q

What are some clinical features of multiple pregnancies

A
  • More marked vomiting in early pregnancy
  • Uterus larger than expected from dates
  • Palpable before 12 weeks
  • Three or more poles felt later in pregnancy
358
Q

Diagnosis of multiple pregnancy

A

Ultrasound

359
Q

What are some maternal complications of multiple pregnancy

A

All obstetric risks are exaggerated in multiple pregnancies

  • Gestational diabetes
  • Pre-eclampsia
  • Miscarriage and preterm delivery
  • IUGR
  • Anaemia
    • Greater increase in blood volume and more demeand for iron and folic aicd
  • Congenital abnormalities
  • Antepartum and postpartum haemorrhage
  • Malpresentation
  • TTTS in MC twins only
360
Q

What are some foetal antenatal compliocations in all multiple pregnancies

A

Complications are due to preterm delivery, IUGR, and monochorionicity

  • Mortatlity (6x)
  • Long-term handicap (5x)
    • Triplets 18x
  • Miscarriage
    • 1st trimester death and late miscarriages
  • Preterm delivery
  • IUGR
  • Congenital abnormalities
361
Q

What are the complications of monochorionicity in multiple pregnancies

A

Result from shared blood supply in the single placenta

  • Twin-Twin Transfusion Syndrome (TTTS)
  • Twin anaemia polycythaemia sequence (TAPS)
  • Twin Reversed arterial perfusion (TRAP)
  • IUGR
  • Co-twin death
362
Q

Describe the pathophysiology ot twin-twin transfusion syndrome (TTTS). What types of twins can this only occur in

A

Occurs only in MCDA twins

  • Unequal blood distribution through vascular anastomoses of the shared placenta
  • The donor twin is volume depleted and develops anaemia, IUGR and oligohydramnios.
  • The recipient twin becomes volume overloaded and may develop polycythaemia, cardiac failure, massive polyhydramnios (in extremis, causes massive distension of uterus)
363
Q

What does the donor twin in TTTS develop?

A
  • Anaemia
  • IUGR
  • Oligohydramnios
364
Q

What does the recipient twin in TTTS develop

A
  • Volume overloaded
  • Polycythaemia
  • Cardiac failure
  • Polyhydramnios
365
Q

How is TTTS staged

A

Quintero staging (1-5)

III - absent or reversed end-diastolic flow in the umbilical artery, pulsatile uymbilical venous flow, reverse ductus venosus flow

366
Q

In TTTS, both twins are ate very high risk of what two complications

A
  • In utero death
  • Severely pre-term delivery
367
Q

Define the features of Twin Anaemia Polycythaemia Sequence (TAPS)

A
  • Occurs when there is marked Hb differences between MC twins but in the absence of liqour volume changes characterisitic of TTTS
  • These occur due to small placental anastomoses, following incomplete laser ablation for TTTS
368
Q

Describe the pathophysiology of Twin Reversed Arterial Perfusion (TRAP)

A

Rare abnormality in MC twins

  • Abnormal, acardiac foetus, perfused by a normal ‘pump’ twin
  • Oxygenated blood comes in from UV into fRV. Deoxygenated blood come out of the pump twins UA into the acardiac foetus UA through anastomoses in placental bed.
  • This blood then leaves acardiac foetus through its UV back into the placenta
369
Q

In TRAP, the pump twin is a t risk of what

A

cardiac failure

370
Q
  • Intrauterine growth restriction is more common in MC twins, in the absence of clear blood volume discordancy.
  • A particular problem is where the umbilical arterywaveform of the smaller twin is very erratic (selective IUGR with intermittent absent or reversed end-diastolic flow, abbreviated to sIUGR with iAREDF).
  • This may be the result of the superficial artery–artery anastomoses, shown in Fig. 27.4; an ultrasound of these is shown inFig. 27.5.
  • Sudden in utero death occurs in up to 20%, handicap in 8%.
A
  • Intrauterine growth restriction is more common in MC twins, in the absence of clear blood volume discordancy.
  • A particular problem is where the umbilical artery waveform of the smaller twin is very erratic (selective IUGR with intermittent absent or reversed end-diastolic flow, abbreviated to sIUGR with iAREDF).
  • This may be the result of the superficial artery–artery anastomoses, shown in Fig. 27.4; an ultrasound of these is shown inFig. 27.5.
  • Sudden in utero death occurs in up to 20%, handicap in 8%.
371
Q

Co-twin death: If one of an MC twin pair dies, due to TTTS or any other cause, the drop in its _____ _____ allows acute transfusion of blood from the other twin. This rapidly leads to _____ and, in about 30% of cases, death or _____ damage. The survivor of a dichorionic twin pregnancy is not at risk, except of _____ _____, because the circulation is not shared.

A

Co-twin death: If one of an MC twin pair dies, due to TTTS or any other cause, the drop in its Bloood pressure allows acute transfusion of blood from the other twin. This rapidly leads to hypovolaemia and, in about 30% of cases, death or neurological damage. The survivor of a dichorionic twin pregnancy is not at risk, except of preterm delivery, because the circulation is not shared.

372
Q

In monochorionic monoamniotic twins, the _____ are always _____. In utero _____ is common, probably because of this and/or sudden acute _____ of blood between the two babies in anastomoses between the close cord insertions

A

In monochorionic monoamniotic twins, the cords are always tangled. In utero demise is common, probably because of this and/or sudden acute shuinting of blood between the two babies in anastomoses between the close cord insertions

373
Q

In ultrasound of dichorionic twins, what sign can be seen

A
  • Lambda sign
  • Dividing membrane is thicker as it meeths the placentas.
  • Remembe dichorionic twins form when fertilised egg divides early
374
Q

In monochorionic twins, what sign is seen on ultrasound

A
  • T sign
  • The dividing membrane is thinner as it meets the placentas
  • Remember monochorionic twins form when fertilised egg divides later
375
Q

Are multiple pregnancies high or low risk pregnancies

A

High risk pregnancies, consultant-led

  • Iron and folic acid supplementation
  • Low dose aspirin if other RF for pre-eclampsia
376
Q

Twins of _____ gender are always _____

A

Twins of opposite gender are always Dizygotic

377
Q

Identification of risk of preterm delivery: Transvaginal
ultrasound of _____ length is not advised in the UK
but may identify those at most risk. In contrast to singletons, neither progesterone nor cervical _____ prevents _____ _____ in multiple pregnancies.

A

Identification of risk of preterm delivery: Transvaginal
ultrasound of cervical length is not advised in the UK but may identify those at most risk. In contrast to singletons, neither progesterone nor cervical cerclage prevents preterm** **birth in multiple pregnancies.

378
Q

How is IUGR monitored in multiple pregnancy

A
  • More difficult to identify vs singleton pregnancies
  • Serial ultrasound examinations performed at 28, 32, 36 weeks and more often with monochorionic twins
379
Q

When is devliery recommended for multiple pregnanciees

A
  • 37 weeks
    • Dichorionic twins
  • 36 weeks
    • Uncomplicated monochorionic twins
380
Q

In monochorionic twins, when does ultrasound surveillance start and what features are we looking out for

A
  • Start 12 weeks and scan every 2 weeks until 24 weeks, at which it should be 2-3 weekly
  • Features:
    • TTTS (16-24 weeks)
      • growth
      • liqour volume discordances
      • Polyhydramnios
      • Tricuspid reguritation (overload)
381
Q

How can mild TTTS be managed

A
  • Laser ablation of the entire placental interfacce in a foetal medicine centre using ultrasound and foetoscopy

Survival both twins 50%, one twin 80%

382
Q

How is high order multiple pregnancy managed

A
  • Selective reduction to twin pregnancy at 12 weeks
    • Needs discussion
    • Balance between increased early miscarriage rates and reduced preterm birth (therefore cerebral palsy)
    • Safest before 14 weeks
  • Surveillance according to chorionicitiy
  • Deliver by 36 weeks
383
Q

What are the indications for the different modes of delivery in multiple pregnancies

A
  • Vaginal delivery - if first foetus is cephalic, regardless of second’s lie or presentation
  • C-section - if first foetus is breech or transverse lie. With high order multiple pregnancies. If there have been antepartum complications. (some places - all monochorionic twins)
384
Q

What considerations need to be had when delivering multiple pregnancies

A
  • When to deliver 37 weeks (DC) or 36 weeks (MC)
  • continious CTG
  • Contractions diminish after first baby delivered - can give oxyitocin if contractions dont start again
  • ECV of second twin can pe performed if not longiutuidinal
  • If foetal distress or cord prolapse, delivery can be expedited with ventouse or breech extraction
  • Prophylactic oxytocin to prevent PPH
385
Q

What are some pitfalls of delivering twins

A
  • Scaring the mother (too mamny people present)
  • Failure to monitor second twin properly
  • Overstimulation of uterus with oxytocin
  • Early rupture of membranes
  • PPH
386
Q

Define a breech presentation

A
  • Foetus presents buttocks or feet first (rather than cephalic presentation - head)
  • Breech delivery has higher perinatal mortality and morbidity (due to birth asphyxia/trauma, prematurity, congenital malformations)
387
Q

Name and describe the types of breech presentation

A
  • Complete (flexed) breech
    • Both legs are flexed at hips and knees
    • Foetus sitting cross-legged
  • Frank (extended) breech
    • Both legs are flexed at the hip and extended at the knee
    • Most common type of breech presentation
  • Footling breech
    • Onr or both legs are extended at the hip
    • foot is presenting part
388
Q

What are some uterine risk factors for breech presentation

A
  • Multiparity
  • Uterine malformation (septate uterus)
  • Fibroids
  • Placenta praevia
389
Q

What are some foetal risks of breech presentation

A
  • Prematuritty
  • Macrosomia
  • Polyhydramnios
  • Twin pregnancy (or higher order)
  • Abnormality (anencephaly)
390
Q

At what gestational age does a breech presentation have limited and important significance

A
  • Limited = 32- 35 weeks
    • Likely to revert to cephalic presentation before delivery
  • Important = >37 weeks
391
Q

How is breech presentation identified and describe features

A
  • Clinical examination
    • Palpation of abdoman - round foetal head in upper part of uterus and irregular mass (foetal buttock and legs) in pelvis
    • Foetal heart auscultated higher on maternal abdomen
  • 20% not diagnosed until labour
    • Vaginal examination - sacrum or foot may be felt through the cervical opening
392
Q

What sign of foetal distress is seen on breech presentation during labour

A

Meconium stained liqour

393
Q

Differential diagnosis for breech presentation

A
  • Oblique lie
  • Transverse lie
  • Unstable lie
394
Q

Investigations for breech presentation

A
  • Ultrasound scan
    • Reveal type of breech
    • Identify foetal or uterine abnormalities that predisposes the breech presentaiton
395
Q

Management options for breech presentation

A
  • External cephalic version
  • Caeserian section
  • Vaginal breech birth
396
Q

Describe how external cephalic version is used to manage breech presentation

A
  • Manipulation of ofetus to cephalic presentation through maternal abdomen
    • If successful -> vaginal delivery
    • 40% success in primiparous, 60% in multiparous
397
Q

Complications of ECV in breech presentations

A
  • Transient foetal hear abnormalities (revert ot onrmal)
  • Persistent hear rate abnormalities (fetal bradycardia) -rarer
  • Placental abruption -rARE
398
Q

Contraindications of ECV in breech presentation

A
  • Recent antepartum haemorrhage
  • Ruptured membranes
  • Uterine abnormalities
  • Previous C-Section
399
Q

When is C-section indicated in breech presentation

A
  • If ECV is unsuccessful, contraindicated or declined by woman
  • Based on evidence that higher perinatal mortality and morbidity in planned vaginal breech biorths vs c-section in term babies
400
Q

Contraindications to vaginal breech birth

A
  • Footling breech
    • Shoulders or head can become trapped in non-fully dilated cervix
401
Q

What is the most important thing to remember in a vaginal breech delivery

A
  • Hand off the breech
  • Traction on baby during delivery can cause feotal head to extend, getting trapped in delivery
  • Foetal sacrum needs to be maintained anteriorly, which is done by holding foetal pelvis
  • If baby does not deliver spontaneously, maneouvres may be required
402
Q

If spontanoues vaginal devliery does not occur in vaginal breech delivery, what maneouvres can be used and describe them

A
  • Flexing foetal knees
    • enables delivery of legs
  • Loovsett’s maneouvre
    • Rotate the body and deliver shoulders
  • Mauriceau-Smellie-Veit (MSV) maneouvre
    • Delivery of head by flexion
    • if MSV fails, forceps can be used
403
Q

Complications of breech presentation

A
  • Cord prolapse
    • Cord drops down below presenting part of baby and becomes compressed
  • Foetal head entrapment
  • PROMs
  • Birth asphyxia
    • Secondary to delay in delivery
  • Intracranial haemorrhage
    • Rapid compression of head during delivery
404
Q

Define foetal lie and name examples

A
  • Relationship between the long axis of of foetus and the mother
    • Longitudinal
    • Transverse
    • Oblique
405
Q

Define foetal presentation and examples

A
  • The foetal part that first enters the maternal pelvis
    • Cephalix vertex = most common and safest
    • Breech
    • Shoulder
    • Face
    • Brow
406
Q

Define foetal position and describe examples

A
  • Position of foetal head as it exits the birth canal
    • Usually head angages in the occipito-anterior position (foetal occiput facting anteriorly)
      • Ideal for birth
    • Occipito-posterior
    • Occipito-transverse

Right is vertex presentation

407
Q

What are some risk factors for abnormal foetal lie, malpresentation and malposition

A
  • Prematurity
  • Multiple Pregnancy
  • Uterine abnormalities (fibroids, partial septate uterus)
  • Foetal abnormalities
  • Placenta praevia
  • Primiparity
408
Q

How is foetal lie identified

A

abdominal examination

409
Q

How is foetal presentation identified

A

abdominal examination

410
Q

How is foetal position ascertained

A

Vaginal examination

411
Q

When identifying foetal lie and presentation, what facotrs might prevent you from identifying either features

A
  • High maternal BMI
  • Full bladder
  • Small foetus
  • Polyhydramnios
412
Q

In terms of lie, presentation and position, what is most favourable

A
  • Longitudinal
  • Cephalic vertex
  • Occipito-anterior position
413
Q

How are abnormal lies or malpresentation invesitigated

A

Confirmed by ultrasound scan

Could demonstrate predisposing uterine or foetal abnormalities

414
Q

Management of abnormal foetal lie

A
  • External cephalic version between 36-38 weeks
415
Q

Management of malpresentation

A

Dependent on the presentation

  • Breech - attempt ECV, vaginal breech delivery or C-Section
  • Brow - C-section
  • Face
    • Chin anterior (mento-anterior) normal labour possible
      • Likley prolonged and risk of C-section being required
    • Chin posterior (mento-posterior) C-section
  • Shoulder - C-section

Bascially C-section except for breech (ECV then C-section/Breech vaginal delivery) or Mento-anterior face presentation

416
Q

Management of malposition

A
  • 90% spontaneously rotate to occipito-anterior as labour progresses
  • If foteal head does not rotate -> rotation and operative vaginal delivery can be attempted
  • C-section is alternative
417
Q

What is amniotic fluid comprised of

A
  • Foetal urine output
  • Small contributions from placenta
  • Small contributions from foetal secretions (respiratory)
418
Q

Describe the normal evolution of amniotic fluid volumes

A
  • Amniotic fluid volume increases steadily until 33 weeks gestation
  • Plateaus 33-38 weeks and then declines
  • Volume at term ~ 500mL
419
Q

Describe the physiology involved in the changing amniotic fluid volumes

A
  • Foetus breathes and swallows amniotic fluid
  • Gets processed, fills bladder and voided
  • Cycle repeats
  • Problems with any structures on this pathway can lead to too much or too little fluid
420
Q

Define oligohydramnios

A
  • Low level of amniotic fluid during pregnancy
  • Amniotic fluid index < 5th centile for gestational age
  • 4.5% term pregnancies
421
Q

Causes of oligohydramnios

A

Anything that reduces foetal urine production, output blockade or rupture of membranes

  • P-PROM
  • Placental insufficiency
    • Blood flow redistribution to foetal brain rather than abdomen and kidneys. Poor urine output
  • Renal agenesis (Potter’s Syndrome)
  • Non-functioning foetal kidneys
    • Bilateral multicystic dysplastic kidneys
  • Obstructive uropathy
  • Genetic/chromosomal anomalies
  • Viral infections
    • Can also cause polyhydramnios
422
Q

How is oligohydramnios diagnosed and what two measurements can be made - describe them

A

Ultrasound examination

  • Amniotic fluid index
    • Measuring cord-free vertical pocket of fluid in four quadratns of uterus and adding them together
  • Maximum pool depth
    • Vertical measurement in any area

Both have similar diagnostic accuracy but AFI is more commonly used

423
Q

Oligohydramnios is diagnosed by ultrasound examination. Therefore, clinical assessment of patyient is directed at establishing the underlying cause. What features in your assessment could point you towards the cause

A
  • History
    • Symptoms of leaking fluid
    • Feeling damp all the time
    • New urinary inctontinence
  • Examination
    • Symphysis fundal height
    • Speculum examination - pooling of liqour
  • Ultrasound
    • Liqour volume, structural abnormalities, renal agenesis, obstructive uropathy
    • Foetal size
      • Small babies result from placental insufficiency which causes oligohydramnios
      • Rise in pulsatility index of umbilical artery doppler in placental insuffieicney
  • Karytopying
    • Early and unexplained oligohydramnios
  • IGFBP-1 in vagina
    • If suspecting ruyptrued membrane
    • Found in amniotic fluid, if positive = strongly suggestive of membrane rupture
424
Q

Management of oligohydramnios is dependent on what

A

Dependent on the underlying cause. Most common two causes are:

  • Rupture of membranes
  • Placental insufficiency
425
Q

Management of oligohydramnios (2o to ruptured membranes)

A
  • Labour likely to comence in 24-48 hours
  • in P-PROM (<37 weeks) IOL considered 34-36 weeks in absence of infection
    • Course of steroids fro foetal lung development
    • Antibiotics to reduce ascending infection
426
Q

Managmenet of oligohydramnios (2o to placental insufficiency)

A
  • Deliver, which is dependent on:
    • Rate of foetal growth
    • Umbilical artery and middle cerebral artery doppler scans
    • CTG
  • Likely delivered <36-37 weeks
427
Q
  • Oligohydramnios in the _____ trimester carries poor prognosis. In these cases, there is PROM+/- infection, with subsequent _____ delivery and pulmonary _____ (lead to respiratory distress at birth
  • Oligohydramnios associated with _____ _____ carries higher rate of preterm deliveries (usually through planned IOL). These have _____ prognosis than that of normal growing foetus
  • Amniotic fluid allows foetus to move its limbs in utero (exercise). Without this, the foetus can develop severe _____ _____- which may lead to _____ despite physiotherapy after birth
A
  • Oligohydramnios in the second trimester carries poor prognosis. In these cases, there is PROM+/- infection, with subsequent premature delivery and pulmonary hypoplasia (lead to respiratory distress at birth
  • Oligohydramnios associated with placental** **insufficiency** carries higher rate of preterm deliveries (usually through planned IOL). These have **poorer prognosis than that of normal growing foetus
  • Amniotic fluid allows foetus to move its limbs in utero (exercise). Without this, the foetus can develop severe muscle** **contractures** - which may lead to **disability despite physiotherapy after birth
428
Q

Most common cause of oligohydramnios

A

Premature rupture of membranes (PROMs)

Treatment is by optimising gestation of delivery

429
Q

Define polyhydramnios

A
  • Abnormally large level of amniotic fluid during pregnancy
  • Amniotic fluid index > 95th centile for gestational age
430
Q

Causes of polyhydramnios

A
  • Idiopathic 50-60%
  • Any condition that prevents foetus from swallowing
    • Oesophageal atresia, CNS abnormalities, muscular dystrophy, congenital diaphragmatic hernia obstructing oesophagus
  • Duodenal atresia
    • Double bubble sign on USS
  • Anaemia
    • Alloimmune disorders, viral infection
  • Foetal hydrops
  • TTTS
  • Increased lung secretions
    • Cystic adenomatoid malformation of lung
  • Genetic or chromosomal abnormalities
  • Maternal diabetes
  • MAterna lithium
    • Foetal diabetes insipidus
  • Macrosomia
    • Large babies produce more urine
431
Q

How is polyhydramnios diagnosed

A

Ultrasound scan (with amniotic fluid index and/or maximum depth pool)

432
Q

Polyhydramnios is diagnosed by ultrasound scan. The clinical assessment is directed at establishing the underlying cause. What are some features of the assessment that may identify the cause

A
  • Examination
    • Tense uterus on palpation
  • Ultrasound scan
    • Measurement of liqour volume
    • Assess foetal size
    • Assess foetal anatomy (structural causes)
    • Doppler - foetal anaemia
  • Maternal GTT
    • GDM or maternal DM
  • Karyotypiung
  • Viral infections (TORCH)
  • Maternal red cell antibodies
    • at 28 weeks
433
Q

Management of polyhydramnios

A

No medicla intervention in majortiy of women

  • Maternal symptoms (breathlessness)
    • Amnioreduction
      • Associated with infection and placental abruption
      • Not performed routinely
  • Indomethacin
    • Enhance water retnetion and reduces foetal urine output
    • Premature closure of ductus arteriosus. DO NOT use beyond 32 weeks
  • Idiopathic polyhydramnios
    • Baby must be examined before first feed to ensure no fistulas or oesophageal atresias
434
Q

Prognosis in pregnancies with polyhydramnios

A
  • Severe and persistently unexplained polyhydramnios = increased perinatal mortality, due to:
    • Presence of underlying abnomralitiy or congenital malformation
    • Increased incidence of preterm labour (due to over-distension of uterus)
435
Q

Complications of polyhydramnios

A
  • Perinatal mortality
  • Malpresentation
    • Transverse lie or breech presentation
    • foetus has more room to move
  • High risk of cord prolapse at rupture of membranes
  • PPH
    • Uteurs has to contract further to achieve haemostasis
436
Q

Urinary tract infections in pregnancy is associated with what complications

A
  • Preterm labour
  • Anaemia
  • Perinatal mortality and morbidity
437
Q

Asymptomatic bacteriuria affects 5% of women but in pregnancy is more likely to lead to what

A

Pyelonephritis (20%)

438
Q

What are some investigations for bacteruria

A
  • Urine culture at booking visit
  • Treat asymptomatic bacteruria at booking
  • Culture if nitrites found on urinalysios
439
Q

Clinical features of pyelonpehritis

A
  • Fever
  • Loin tenderness and abdominal pain
  • Dysuria
  • Rigors
  • Tachycardia
  • Vomitting
440
Q

Management of pyelonephritis

A

IV antibiotics

  • ?Erythromycin/?cephalosporin
441
Q

What is the usual causative organism for pyelonephritis in 75% of cases

A
  • E coli
  • Resistant to amoxiciillin
442
Q

Thyroid status does not alter in pregnancy, although _____ clearance is increased. Goitre is more common. Fetal thyroxine production starts at _____ weeks; before, it is dependent on maternal thyroxine. Maternal thyroid-stimulating hormone (TSH) is _____ in early pregnancy.

A

Thyroid status does not alter in pregnancy, although iodine clearance is increased. Goitre is more common. Fetal thyroxine production starts at 12 weeks; before, it is dependent on maternal thyroxine. Maternal thyroid-stimulating hormone (TSH) is increased in early pregnancy.

443
Q

Most common causes of hypothyroidism in UK

A
  • Hashimoto’s thyroiditis
  • Thyroid surgery (iatrogenic)
  • Iodine defieicny (developing countries)
444
Q

Hypothyroidisim associated with increased risks in

A
  • Perinatal mortality
  • Miscarriage
  • Preterm delivery
  • Intellectual impariemtn in childhoof
  • Pre-eclampsia (esp if anti-thyroid Ab present)
445
Q

Management of hypothyroidism in pregnancy

A
  • Replacement of thyroxine
  • Monitor TSH 6-weekly
446
Q

Common cause of hyperthyroidism

A

Graves disease

447
Q

Untreated hyperthyroidism increases what

A

perinatal mortality

448
Q

Graves disease in pregnancy: Antithyroid antibodies also cross the _____; rarely, this causes neonatal _____ and goitre. For the mother, thyrotoxicosis may improve in late pregnancy but poorly controlled disease risks a ‘_____ storm’ whereby the mother gets acute symptoms and _____ failure. Symptoms may be confused with those of pregnancy.

A

Antithyroid antibodies also cross the placenta; rarely, this causes neonatal thyrotoxicosis and goitre. For the mother, thyrotoxicosis may improve in late pregnancy but poorly controlled disease risks a ‘thyroid storm’ whereby the mother gets acute symptoms and heart failure. Symptoms may be confused with those of pregnancy.

449
Q

Hyperthyroidism in pregnancy treated with?

A
  • Propylthiouracil (PTU) in 1st trimester
    • Instead of carbimazole
    • PTU crosses placenta
    • Can sometimes cause neonatal hypothyroidism
    • Lowest possible dose used
    • TFT tested monthly
  • Grtaves worsens post-partum
450
Q

What is a common cause of postnatal depression

A

Postpartum thyroiditis

common 5-10%

451
Q

Risk factors for postpartum thyroiditis

A
  • Antithyroid antibodies
  • Type 1 diabetes
452
Q

Describe the evolution of postpartum thyroiditis

  • Transient and usually subclinicaly _____(hyper/hypo)thyroidism, usually about _____ months post-partum
  • this is followed by _____ months of _____(hyper/hypo)thyroidism
  • Permanent in 20%
A
  • Transient and usually subclinical hyperthyroidism, usually about 3 months post-partum
  • this is followed by 4 months of hypothyroidism
  • Permanent in 20%
453
Q

What is the most important route of transmission of HIV in pregnant women

A

Heterosexual intercourse

454
Q

What are some maternal effects of HIV in pregnancy

A
  • Pre-eclampsoa
  • GDM
455
Q

What are some neonatal/foetal effects of HIV in pregnancy

A
  • Stillbirth
  • pre eclampsia
  • Growth restriction
  • Prematurity
456
Q

When is the risk of HIV transmission highest in pregnancy

A
  • Beyond 36 weeks
  • Intrapartum
  • Breastfeeding
457
Q

What are some factors that increase the risk of transmission of HIV

A
  • Low CD4 counts
  • High viral load
  • Coexistent infection
  • Premature delivery
  • Intrapartum
  • Prolonged rupture of membranes >4 hours
458
Q

Management of HIV in pregnancy

A

Screening and prophylaxis

  • Screened at booking
  • STI and PCP surveillance
  • LFTs and renal function (drug toxicity)
  • Hb and glucose monitoring

Preventing transmisison

  • Control viral load with HAART
    • Continued throughout pregnancy and delivery
  • Neonate treated with PeP for first 6 weeks
  • If woman was not on treatment pre-pregnancy, then start therapy at 28 weeks
  • C-section ig viral load >50 copies/mL and co-existing Hep C infection
  • Avoid breastfeedging
459
Q

Define female genital mutiltaion

A
  • Female circumcision
  • Partial or total removal of external female genitalia or other injury to the female genital organs for non-medical reasons
  • Practised in Africa and Middle East, Malaysia and Indonesia for different reasons, including ideas of preservation of virginity, promoting hygeine, adherence to cultural norms and religion - FGM is not condoned in the Bible or the Koran
  • Violation of human rights, child abuse and has no health benefits
460
Q

What are the classifications of FGM

A

Type 1

  • Clitoridectomy
  • Partial or total removal of the clitoris, or of the prepuce

Type 2

  • Excision
  • Partial or total removal of the clitoris and the labia minora ± the labia majora

Type 3

  • Infibulation
  • Narrowing of the vaginal opening by cutting and repositioning the labia, with or without removal of the clitoris

Type 4

  • Other
  • All other non-medical procedures to female genitalia for non-medical purposes (?peircings)
461
Q

Complications of FGM

A
  • Short term
    • Pain, bleeding, infection, urinary retention, damage to pelvic organs, death
  • Longer term
    • Failure to heal, UTI, difficulty urinating/menstruating, chronic pelvic infection, vulval pain (cysts and neuromas), dyspareunia, infertility, fistula, severe perineal trauma during childbirth
    • Psychological
462
Q

FGM and the law: True or false

  • In the UK it is illegal to perform FGM, including reinstatement after vaginal birth, or to arrange for FGM to happen.
  • It is illegal to take or arrange for a girl to be taken to another country for FGM, even if it is legal in that country.
  • Female children may be at risk of FGM and healthcare workers have a statutory duty to safeguard them.
A
  • In the UK it is illegal to perform FGM, including reinstatement after vaginal birth, or to arrange for FGM to happen. - TRUE
  • It is illegal to take or arrange for a girl to be taken to another country for FGM, even if it is legal in that country. -TRUE
  • Female children may be at risk of FGM and healthcare workers have a statutory duty to safeguard them. - TRUE
463
Q
A