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RANZCOG 2024 - Antenatal > Growth, Liquor, Dopplers > Flashcards

Growth, Liquor, Dopplers Flashcards

1
Q

Discuss uterine artery dopplers
-When to measure (2)
-Who to measure on (2)
-What it measures (3)
-What is abnormal (2)
-How it should be used in management (5)

A
  1. When to measure
    -20 - 24 weeks gestation
    -If abnormal at 20 weeks repeat at 24 weeks
  2. Who to measure
    -Women at risk of SGA and PET, current HTN disorder
  3. What it measures
    -Shows flow resistance on maternal side of the placenta
    -Suggests maternal cause for growth restriction
  4. What is abnormal
    -Notching after 24 weeks
    ->95% percentile is abnormal
    5 How it can be used in management
    -Can be used to at time of diagnosis of SGA
    -Helps predict risk of early onset IUGR
    -Can help differentiate the SGA from IUGR babies
    -If abnormal offer serial growth scans
    -If normal offer third trimester growth scans
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2
Q

Discuss the pathophysiology of uterine artery dopplers

A

-Defective replacement of spiral arteries by trophoblasts results in failure to convert high resistance maternal arteries into low resistance channels resulting in poor blood supply to placenta and therefore fetus

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3
Q

Discuss umbilical artery dopplers
-When to measure (7)
-When should it not be done
-What it measures
-How to use in pregnancy
5. What is the frequency of doppler investigation

A
  1. When to measure
    -SGA baby
    -EFW <10th
    -EFW dropped by >30 centiles
    -AC less than 5th centile on population chart
    -Discrepancy between head and abdo circumference > 30% with AC being lower
    -Maternal HTN disorder
    -Decreased FM
  2. When should it not be done
    -In normal pregnancies with no maternal or fetal risk factors
  3. What does it measure
    -Provides information about the fetal side of the placenta.
    -Reflects downstream resistance at the placental stem and terminal villi
  4. Use in pregnancy
    -Primary surveillance screen in SGA
    -Use has been shown to reduce perinatal mortality (Cochrane review)
    -Use shows reduced CS and IOL if used
  5. Frequency of doppler
    -If SGA/IUGR and normal UAPI do fortnightly
    -If SGA/IUGR and abnormal UAPI do twice weekly
    -If SGA/IUGR and abnormal with AEDF or REDF do daily
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4
Q

Discuss umbilical artery dopplers
-Pathophysiology
-Progression
-What is an abnormal UAPI

A
  1. Pathophysiology
    -Abnormal spiral artery remodelling leads to prolonged reduction in maternal intervillous perfusion
    -Leads to reduced oxygen delivery to the fetal surface of the placenta
    -Results in vasoconstriction of the stem villi
    -Results in increased resistance to flow from fetus to the placenta
  2. Progression
    -Usually the resistance in the umbilical arteries drops as gestation increases
    -30% of villous vascular dysfunction = increased UAPI
    -60% of villous vascular dysfunction = AEDF/REDF
    -In early onset IUGR with abnormal dopplers the time between AEDF and REDF may be weeks
    -In third trimester the interval between AEDF and REDF is shorter
  3. Abnormal UAPI = >95%
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5
Q

How should umbilical artery doppler be measured (6 points)

A
  1. Perform when baby is not moving
  2. Always keep Tlb <0.5 by reducing acoustic power output
  3. Identify free loop of umbilical cord
  4. Try to position the beam so the blood flow is parallel or at least has an angle less than 60 degrees
  5. Get spectral trace
  6. Freeze image when 5 symetrical wave forms have been obtained
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6
Q

Describe the umbilical wave forms for
1. Normal pregnancy
2. Reduced end diastolic flow
3. Absent end diastolic flow
4. Reversed end diastolic flow

A
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7
Q

Discuss middle cerebral artery dopplers
-When to measure (3)
-What it measures (5)
-Use in pregnancy (3)
-What is an abnormal MCA

A
  1. When to use
    -SGA/IUGR and >34weeks regardless of UAPI
    -SGA/IUGR and <34 if UAPI abnormal
  2. What it measures
    -Measures fetal brain arterial circulation.
    -Normally shows high resistance pattern
    -Low resistance pattern abnormal
    -Reflects chronic hypoxia not acidemia
    -Correlates poorly with acidemia at birth
  3. Use in pregnancy (No longer used in NZ)
    -If <34 weeks do not use to time delivery
    -If>34 weeks time delivery at 38-39 weeks
    -If abnormal chance of CS 68%
  4. Abnormal MCA PI <5th centile
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8
Q

Discuss the pathophysiology of middle cerebral artery doppler

A

-Placental insufficiency leads to chronic hypoxia
-Brain arteries vasodilate to enhance local perfusion
-Resistance in vessels drops
-Once resistance as low as possible the MCA is no longer useful to predict worsening hypoxia
-Normalisation of MCA can reflect auto regulatory dysfunction as fetus no longer responding appropriately to hypoxic environment - be worried if MCA normalises and everything else abnormal

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9
Q

Discuss cerebral placental ratio
-When to measure
-What it measures
-Use in pregnancy (now used in NZ for timing)
-What is an abnormal CPR

A
  1. When to measure
    -If MCA is performed then CPR should be calculated
  2. What it measures
    -Is a ratio of MCA: UAPI
    -Represents fetal blood flow redistribution
    -Predicts redistribution of cardiac output relative to cerebral blood flow
  3. Use in pregnancy
    -Might be useful in predicting at risk fetus whose individual parameters are normal
    -May be useful in predicting baby’s that don’t tolerate labour
    -If abnormal 58% chance of CS
    -Ass with fetal distress, CS and NICU admission
  4. Abnormal CPR = <5th centile
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10
Q

Discuss ductus venosus doppler
-When to measure (2)
-What it measures
-Use in pregnancy

A
  1. When to measure
    -Abnormal dopplers <32 weeks
  2. What it measures
    -Flow through the ductus venosus which shunts blood from the umbilical vein to the IVC bypassing the liver
    -Provides information about severe hypoxia and caridac health.
    -Is a late sign of things going badly if abnormal
  3. Use in pregnancy
    -Best predictor of acidemia at birth in early onset fetal growth restriction
    -Should be used to time delivery in SGA/IUGR babies who are preterm <32/40
    -Deliver when there is an absent a wave indicating absent or reversed flow (Truffle trial)
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11
Q

Discuss ductus venosus dopplers
-Pathophysiology
-What is abnormal

A
  1. Pathophysiology
    -Increasing arterial resistance leads to poor myocardial contractility and increased R heart pressures (effectively heart failure driven by HTN).
    -Increased R heart pressure leads to reduced diastolic flow in the ductus venosus
    -Reduced flow from DV means less oxygenated blood which results in increased DV dilatation to allow for increased blood flow
    -Leads to loss of a wave
  2. Abnormal findings
    -DVPI is abnormal when >95%
    -Absent A wave (Late finding)
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12
Q

Discuss MCA PSV doppler
-Indications
-How to interpret
-What it measures

A
  1. Indications
    -Maternal fetal isoimmunisation
    -Any suspicion of fetal anemia
    -Unexplained hydrops
    -MCDA twins >24 weeks gestation
    -MCDA twins with known TTTS or TAPS
  2. How to interpret
    ->1.5Mom is abnormal
    -Differs with gestational age (MCA PSV increases)
  3. What it measures
    -A measure of anaemia
    -Based on increased blood flow from increased cardiac output and reduced blood viscosity
    -Predicts moderate to severe anaemia
    -False positive rates increase after 35/40
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13
Q

Discuss fetal hydrops
-Definition (2)
-Incidence (2)
-Prognosis (4)

A
  1. Definition
    -Excessive extravascular fluid accumulation
    -Diagnosed by 2 or more of
    -Pericardial effusion
    -Pleural effusion
    -Ascites
    -Skin oedema
    -Polyhydramnios
    -Placental enlargement
  2. Incidence
    -1:1500 - 3500
    Ratio of non-immune to immune 9:1
  3. Prognosis
    -50-70% overall
    -100% if associated with structural heart defect / TTTS / chromosomal abnormality
    -Live birth rate 40-60%
    -Those born alive have 60% chance of normal developmental outcomes
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14
Q

What are the causes of hydrops (6 groups)

A
  1. Immune
    -Red blood cell alloimmunisation resulting in fetal haemolytic anemia
  2. Chromosomal
    -Turners, T21/13/18
  3. Haematological
    -Thalassemia (Barts hydrops)
    -Anaemia
    -TTTS
  4. Infection
    -Parvovirus, CMV, Toxoplasmosis
  5. Metabolic
    -Glucose-6-phosphate dehydrogenase deficiency
    -Pyruvate kinase deficiency
  6. Structural
    -Cardiac - primary cardiac failure, secondary cardiac heart failure
    -Thoracic CPAM, congenital diaphragmatic hernia
    -GIT - oesophageal atresia
    -Renal - Low urine output from renal agenesis / obstruction
    -Lymphatic obstruction
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15
Q

Discuss the pathophysiology of hydrops

A

Causes of hydrops feed into three main outcomes
-Endothelial failure = increased capillary leakage
-Liver failure = decreased oncotic pressure
-Heart failure = increased central venous pressure
These things result in increased fluid in the tissue

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16
Q

How should hydrops be investigated (7)

A

-Maternal blood group and screen for HDN antibodies
-Kliehauer to assess maternal fetal haemorrhage
-MCA PSV to assess fetal anaemia
-Maternal serology for infection
-Amnio for karyotype
-Fetal tertiary anatomy scan and echo for fetal heart defects
-Consider fetal blood sampling

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17
Q

How should hydrops be managed
-Antenatal (5)
-Delivery (4)
-Postpartum (3)

A
  1. Antenatal management
    -Management depends on cause
    -Consider intrauterine fetal transfusion if cause is fetal anaemia
    -Transplacental anti-arrythmics if cause is fetal arrythmia
    -Drainage of pleural effusions to prevent lung hypoplasia
    -Laser photocoagulation of placental anastomosis in TTTS
  2. Intrapartum management
    -Delivery if maternal health at risk (PET)
    -Consider delivery after 34 weeks
    -Needs to be case by case
    -Choice of delivery case by case
  3. Postnatal management
    -Deliver at a place with NICU. Will likely need resus
    -Drain effusions
    -Investigate for possible causes
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18
Q

Discuss maternal implications of fetal hydrops

A

-Fetal hydrops from any cause can result in maternal symptoms
-Can mimic PET or nephrotic syndrome
-Generalise oedema that mimics fetal sites of oedema
-Can occur at anytime and may persist postpartum but usually resolves
-Severe maternal complications in 21%
-Reversal of fetal hydrops or fetal demise reverses maternal symptoms
-Usually warrants prompt delivery as can deteriorate rapidly

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19
Q

Discuss fetal macrosomia
-Definition (3)
-Prevalence (2)
-Risk factors (10)

A
  1. Definition
    -Macrosomia is >4kg or 4.5kg at any gestation
    -No universally accepted definition
    -LGA = Birth weight >90%
    -RANZCOG guideline uses EFW/AC >95%
  2. Prevalence
    - 9% >4kg
    - 0.1 >5kg
  3. Risk factors
    -Incorrectly dated gestation
    - Constitutional
    -Maternal diabetes
    -Maternal obesity - 12.7% or 22% if GDM
    -Excessive maternal weight gain
    -AMA >30yrs
    -Post dates
    -Multiparity
    -Previous macrosomic/LGA baby
    -Ethnicity
    -Male fetus
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20
Q

Discuss the risks for macrosomic babies
-To mother (4)
-To fetus (4)
-To neonate (5)
-To child (4)

A

Risks increase for mothers and babies over 4kg weight and sharply after 4.5kg fetal weight.
1. Maternal risks
-Prolonged or obstructed labour
-Increased risk CS (OR 2 if >4.5kg)
-PPH - OR 3
-Chorioamnionitis OR 2.4
-3rd or 4th degree tears OR 1.7
2. Fetal risks
-Shoulder dystocia (OR 7)
-Brachial plexus injury (OR 21. Absolute risk 3-7%)
-Fracture (OR 10)
-Low apgar at 5 mins
3. Neonate
-Hypoglycemia
-Respiratory problems
-Polycythemia
-Minor congenital abnormalities
-Increased admission to NICU
4. Childhood
-Obesity
-Impaired glucose tolerance
-Metabolic syndrome
-Cardiac remodelling

21
Q

Discuss management of Macrosomic babies
-Preconception (5)
-Antenatally (5)
-Intrapartum ()

A
  1. Preconception
    -Aim for prevention
    -Well controlled GDM/diabetes mean BSL <5.6
    -Pre-pregnancy weight loss - consider bariatric surgery (Obesity Class II or III)
    -Avoid excess weight gain in pregnancy
    -Exercise
  2. Antenatally
    -Diagnosis with scan +/- 20% accuracy. Check close to 37-38 weeks
    -Check GDM status
    -Control BSL
    -Encourage healthy weight gain
    -Counsel regarding delivery
  3. Delivery
    -IOL before 39/40 reduces shoulder dystocia RR0.6 and neonatal fractures RR0.2. No difference in CS rates. Increases the risk of neonatal photo therapy requirement.
    -Considering IOL should be shared decision making
    -Evidence is still unclear on IOL >39/40
    -Offer CS if >4.5kg and diabetic
    -Offer CS if >5kg and not diabetic - 79-375 CS to avoid 1 case of permanent brachial plexus injury
    -Careful consideration of instrumental delivery. Increased risk of shoulder dystocia - RR 3
22
Q

Discuss findings from the Cochrane trial for IOL for LGA
-Method (3)
-Outcomes (4)

A

-4 RCT not blinded
-Included 1190 women without GDM
-Compared IOL 37-40 weeks with expectant management
-Increase in fracture with expectant management
-Increase in shoulder dystocia with expectant management
-No difference with brachial plexus injury, apgar scores, CS or instrumental delivery
-Increased risk of perineal damage with IOL

23
Q

Discuss oligohydramnios
-Definition (2)
-Incidence (3)
-Causes (7)

A
  1. Definition
    -SDP <2cm
    -AFI <5cm - Using this definition increased IOL and CS but no difference in outcomes
  2. Incidence
    -1% overall
    -2% by 34 weeks
    -11% by term
  3. Causes
    -Idiopathic - usually at postdates when fetal swallowing > production of fluid
    -Placental insufficiency (PET/Abruption, maternal CKD)
    -Medications - ACEi, NSAIDS
    -Dehydration
    -Fetal renal agenesis, non-functioning kidney, obstructive uropathy
    -Chromosomal abnormalities
    -Infections
    -SROM
24
Q

Discuss polyhydramnios
-Definition (4)
-Incidence (4)
-Timing of onset (2)
-Causes (4 groups/points)

A
  1. Definition
    -SDP 8-11cm = mild, 12-15cm moderate, >16 severe
    -AFI >25cm
  2. Incidence
    -1%
    -80% mild, 15% moderate, 5% severe
  3. Timing of onset
    -2nd Trimester - fetal anomaly, TTTS, maternal medicine condition
    -3rd Trimester - anomalies, diabetes, infection, idiopathic
  4. Causes
    -Most mild polyhydramnios is idiopathic
    -Moderate and severe polyhydramnios has an underlying cause
    -Decreased fetal swallowing - brain abnormalities, structural defects - oesophageal atresia, compression from diaphragmatic hernia,
    -Increased fetal urination - Maternal diabetes, fetal and placental tumours, twin to twin transfusion, things that cause increased cardiac output (fetal anaemia), infection
25
Q

What investigations should be undertaken in pregnancies with polyhydramnios (6)

A
  1. Detailed USS for structural abnormalities
  2. Karyotyping if USS suggestive
  3. OGTT
  4. TORCH screen
  5. USS every 1-3 weeks to monitor fetal condition and fluid levels
  6. MCA PSV if concern for fetal anaemia
26
Q

What are the risks associated with polyhydramnios
-Maternal (5)
-Fetal (7)

A
  1. Maternal risks
    -Maternal discomfort
    -Cardiorespiratory compromise
    -Placental abruption
    -CS delivery due to malpresentation/unstable lie/cord prolapse
    -PPH
  2. Fetal risks
    -PPROM
    -PTB
    -Placental abruption
    -Cord prolapse
    -2-5x risk of perinatal mortality - worst prognosis SGA + poly
    -Increased perinatal morbidity - TTN, hypoglycemia, NICU admission, reduced apgars
27
Q

Discuss treatment of polyhydramnios
-Antenatal
-Delivery

A
  1. Antenatal management
    -Depends on cause of polyhydramnios
    -BSL management in GDM/DM
    -If anaemia - intrauterine blood transfusion
    -TTTS - laser occlusion of placental anastomoses
    -Hydrops from arrythmias - antiarrythmic meds
    -Parvovirus screen
    -TORCH screen only indicated if other USS abnormalities
    -Consider amnioreduction
    -can cause PTL, abruption, infection.
    -Consider after 32/40 with severe respiratory compromise
    -Indomethacin
    -prostaglandin synthetase inhibitor.
    -Results in decreased fetal urination by increasing fetal ADH
    -Can lead to premature closure of PDA, renal dysfunction, intraventricular haemorrhage
    -Monitor polyhydramnios 3 weekly with USS
  2. Delivery
    -IOL by 40 weeks
    -Continuous fetal monitoring
    -Controlled ARM with position confirmation prior
    -Active management for increased risk PPH
28
Q

What are the definitions for the following
-SGA (1)
-Severe SGA (1)
-IUGR (7)
-Low birth weight (1)
-Early onset growth restriction
-Late onset growth restriction

A
  1. SGA
    -EFW or AC <10th centile
  2. Severe SGA
    -EFW or AC <3rd centile
  3. IUGR
    -Fetus fails to meet growth potential
    -EFW / AC < 3rd centile
    -AC / EFW <10th centile +
    -Abnormal dopplers (Uterine or umbillical or CPR)
    -EFW or AC crossing >2 quartiles (ISUOG)
  4. LBW
    - <2.5kg
  5. Early onset growth restriction
    -Onset <32/40
    -Diagnosed if EFW/AC <3rd or AC/EFW <10th and abN UAPI or uterine artery doppler
  6. Late onset growth restriction
    -Onset >32/40
    -Diagnosed if EFW/AC <3rd centile or 2 of the following: EFW/AC <10th; EFW or AC crossing >2 quartiles or AbN dopplers (UtA notching, CPR ,5th UAPI >95th)
29
Q

Describe the characteristics of early onset FGR
-Gestation
-Prevalence
-Association with pre-eclampsia
-Association with placental pathology
-Relation to SGA
-Umbilical artery dopplers
-Ease of detection
-Clinical consequences

A
  1. Gestation
    - <32/40
  2. Prevalence
    - 0.5-1%
  3. Pre-eclampsia
    -Strong association
  4. Placental pathology
    -Strong association
  5. Relation to SGA
    -Often SGA
  6. Umbilical artery dopplers
    - Usually abnormal
  7. Ease of detection
    -Often readily detectable
  8. Clinical consequences
    -Risk of prematurity, high mortality and morbidity
30
Q

Describe the characteristics of late onset FGR
-Gestation
-Prevalence
-Association with pre-eclampsia
-Association with placental pathology
-Relation to SGA
-Umbilical artery dopplers
-Ease of detection
-Clinical consequences

A
  1. Gestation
    >32/40
  2. Prevalence
    - 5-10%
  3. Association with PET
    -Weak
  4. Association with placental pathology
    -Weak
  5. Relation to SGA
    -Not always SGA
  6. Umbilical artery doppler
    -Normal or abnormal
  7. Detection
    -Challenging to detect
  8. Clinical consequences
    -Associated with increased mortality and morbidity
31
Q

What are the outcomes of IUGR babies
-Immediate consequences (10)
-Long term consequences (7)

A
  1. Immediate consequences
    -40% of non-anomalous still births are growth restricted
    -Perinatal mortality RR 3.0 if EFW 5-10th centile
    -Perinatal mortality RR 15.0 if EFW <1st centile
    -Perinatal morbidity - hypoglycemia, jaundice, hypothermia, sepsis, polycythemia, SUDI
    -PTB
  2. Long term consequences
    -Obesity
    -T2DM
    -Cardiovascular disease
    -Neurodevelopment delay
    -Cerebral palsy
    -Lower IQ
    -Short statue
32
Q

What are the causes of IUGR
-Non-placental mediated (5)
-Placental mediated (2 groups)

A
  1. Non-placental mediated - usually early onset
    -Constitutionally small 50-70%
    -Structural anomaly
    -Chromosomal anomaly - 20% picked up by SGA
    -Inborn errors of metabolism
    -Fetal infection - 5% SGA - CMV and toxo most common
  2. Placental mediated - usually late onset
    -Maternal factors (Low / high BMI, poor nutrition, substance abuse, severe anaemia)
    -Medical factors (PET, autoimmune disease, HTN, renal disease, diabetes)
33
Q

Discuss IUGR
-Major risk factors (RR >2) (12)
-Minor risk factors (7)
-Biochemical indicators (1)
-USS indicators
-Examination indicators (2)

A
  1. Major risk factors RR >2
    -Maternal age >40 RR 3
    -Previous SGA baby RR 4
    -Previous still birth RR 6
    -Smoking after 16 weeks RR 2
    -Daily vigorous exercise RR 3
    -Maternal or paternal SGA RR 3
    -Chronic HTN RR 2.5, gHTN severe RR 2.5 / PET (passed or current)
    -Diabetes with vascular involvement RR 6
    -Renal impairment RR 5
    -APLS RR 6
    -Previous HTN
    -PET RR 2 /
    -APH / abruption or heavy early pregnancy bleeding
  2. Minor risk factors RR <2
    - Low maternal weight gain
    -Maternal age > 40
    -IVF
    -Nulliparity
    -BMI outside >30 or <18.5
    -Smoker <10/day
    -Placenta praevia
    -Pregnancy interval <6 months >60 months
  3. Biochemical indicators
    -PAPP-A Major RF if <0.4 MoM (off guideline)
  4. USS indicators
    -Uterine artery doppler >95% or notching
    -60% chance of PET/SGA if abnormal
    -Good at predicting early onset IUGR
  5. Examination indicators
    -SFH measure is good at ruling in SGA if SFH is <10%
    -SFH measure is poor at ruling out SGA if SFH is normal
    -If SFH is <10%, static or slowing evaluate with USS
34
Q

Discuss early management of IUGR (5 points)

A
  1. Screen for risk factors
    -Different guidelines have different procedures
    -Don’t us USS if no major or only 2 or less minor RF (Use serial FH)
    1+ major risk factor - monthly growth scans from 26 weeks (28-30 weeks in NZ) Start 24/40 if risk Early onset IUGR
    3+ minor risk factors - Uterine artery doppler at 20-24 weeks. (NZ suggests scan at 32+36/40)
    -If uterine artery dopplers abnormal - GS from 24 weeks (Do UtA if RF for early onset IUGR)
    -If uterine artery dopplers normal - GS in third trimester
  2. If low risk SGA then no evidence for serial GS
  3. Consider aspirin from 12-16 to 36/40 if
    -Previous SGA
    -High risk PET
    -Maternal medical condition
    -PAPP-a <0.2MoM (Safer baby bundle) - <0.4MoM
    -Two or more other risk factors
  4. Counsel mother on modifiable risk factors
    -Weight gain or loss
    -Increasing birth interval
    -Smoking cessation
    -Substance abuse cessation
    -Limiting vigorous exercise
  5. In early onset or severe IUGR consider screening for infection (CMV, Syphillis, Toxo)
35
Q

Discuss Antenatal management of SGA
-Investigations (7)
-Monitoring (7)
-Considerations (4)

A
  1. Investigations
    -Review for aneuploidy - screening
    -Review anatomy scan for anomalies
    -Tertiary USS if early onset IUGR
    -Karyotype if anomaly detected or early onset <23/40
    -Consider TORCH screen in early onset IUGR
    -Consider syphilis and malaria screen if high risk
    -Blood pressure, urinalysis and PCR if PET suspected
    -Ref to MFM if concern for anomaly or polyhydramnios or Early onset IUGR particularly < 28/40
  2. Monitoring
    USS and charted on customised grow chart. More predictive of outcomes
    UAPI in all gestations
    -If normal GS every 2-3 weeks
    -If raised UAPI clinical review and CTG 2 x weekly, LV and doppler weekly/ twice weekly
    -If Absent / reversed UAPI - admission and daily dopplers + TDS CTG
    MCA PI and CPR
    -If Abnormal UAPI <34/40
    -Always if > 34/40
    DV -If < 32/40 and UAPI abnormal
    CTG
    -Short term variability most predictive of fetal acidemia
    Liquor volume
    -Measure SDP
    Biophysical profile - DON’T use as high false negatives in preterm
  3. Other considerations
    -Avoid metformin if GDM
    -Avoid atenalol
    -Encourage smoking cessation - if stop before 15/40 then SGA risk goes away
    -No evidence for calcium or progesterone
36
Q

Describe the progression of early onset IUGR (8 steps)

A
  1. Raised UAPI
  2. Low CPR
  3. Low MCAPI
  4. Absent end diastolic flow in the umbilical artery
  5. Decreased flow in the ductus venosus
  6. Low short term variability on CTG
  7. Absent or reduced end diastolic flow in the DV
  8. Fetal demise
37
Q

Discuss timing of delivery for IUGR babies
-If absent or reversed EDF
-If abnormal UAPI but forward flow
-If normal UAPI dopplers
-If static growth over 3 weeks
-If short term variability poor

A
  1. Absent or reversed end diastolic flow
    -Check DV if <32 weeks and if abnormal deliver anytime
    -If absent EDF deliver anytime >34 weeks
    -If reversed EDF deliver anytime >32 weeks
  2. Abnormal UAPI with forward flow
    -Deliver by 36 - 38/40 (NZ/ISUOG) / 37/40 (RCOG) or 37/40 if abN MACPI (RCOG)
  3. Normal dopplers
    -Aim delivery at 40 weeks
    -Aim >36/40 if EFW <3rd centile
    -If AbN MCAPI/CPR aim delivery 38/40 (NZ uses CPR)
  4. If static growth >3 weeks
    -Deliver anytime >34 weeks
  5. If STV <3
    -Deliver regardless of dopplers if STV <3 anytime 29-32/40
    -Deliver regardless dopplers if STV <2.6 anytime <29/40
38
Q

Discuss mode of delivery with abnormal dopplers
-If Absent or reversed end diastolic flow
-Other abnormal dopplers
-What is the chance of CS with raised UAPI
-What is the chance of CS with abnormal CPR
-What is the chance of CS with abnormal MCAPI
-What is the safest form of IOL

A
  1. Absent or reversed end diastolic flow
    -CS recommended
    -AEDF 34/40
    -REDF 32-34/40
  2. Other abnormal dopplers
    -IOL - timing depends on dopplers
  3. Chance of CS with raised UAPI - 15%
  4. Chance of CS with abnormal CPR 58%
  5. Chance of CS with abnormal MCAPI 55% offer CS
  6. Safest method of IOL
    Balloon better than PG according to Cochrane review
    -Less hyperstimulation and neonatal morbidity with balloon
    -No difference for CS, VB, maternal morbidity, NICU admissions. PSANZ states increase in VB with balloon
39
Q

Discuss placental pathology and IUGR
1. What are the rare placental pathologies associated with IUGR (3)
2. What is their recurrence rate
3. What type of IUGR are they associated with

A
  1. Types of pathiology
    -Massive perivillous fibrin deposition
    -Chronic intervillositis
    -Villitis of unknown etiology
  2. Recurrence rate
    -High
  3. Type of IUGR
    -Usually seen in early IUGR <32/40 but can occur in late onset IUGR
40
Q

Discuss diagnosis of fetal macrosomia
-Accuracy of SFH (2 points)
-Accuracy of USS (5 points)

A
  1. Accuracy of SFH
    -Poor at picking up macrosomia - sensitivity 20-70%
    -Good at excluding macrosomia
  2. Accuracy of USS
    -Accuracy can be off by 20%
    -Accuracy decreases with increasing fetal weight >4kg
    -Best USS predictor for shoulder dystocia was AC and BPD difference of >2.6cm
    -Universal 3rd trimester screening picks up more macrosomic babies but doesn’t clinically predict shoulder dystocia
    -USS sensitivity 56% and specificity 92% for prediciting fetal weight >4kg
41
Q

What are the RANZCOG recommendations for macrosomic babies (10)

A
  1. Universal third trimester USS finds more macrosomic babies but this does not have a clinically significant effect at predicting shoulder dystocia
  2. USS and SFH should be considered with caution when looking at macrosomia but are good at ruling out macrosomia
  3. Benefits of IOL before 39/40 for babies >95% EFW should be weighed against challenges with USS measurements and short and long term outcomes for babies born <39/40
  4. Can offer ELCS to babies >4.5kg in diabetic mothers and >5kg in non-diabetic mothers
  5. Women with suspected macrosomic babies should be counselled about risks and benefits of MOD.
  6. Decision to proceed with operative birth in babies with suspected macrosomia should be undertaken by an experienced clinician and consider doing in OT
  7. Consider macrosomia when discussing VBAC but macrosomia is not a contraindication to VBAC
  8. Women without contra-indications should be encouraged to participate in exercise to reduce macrosomia
  9. Control of maternal hyperglycemia reduces the risk of macrosomia in diabetic women. Universal GDM screening is recommended
  10. Pre-pregnancy counselling for women class III obesity should include risks and benefits of bariatric surgery
42
Q

Discuss the Truffle trial
-Aim (1)
-Study design (4)
-Primary outcomes (1)

A
  1. Aim
    To determine if changes in DV waveform could be used to trigger delivery instead of CTG in very preterm IUGR
  2. Study design
    -Multicentre RCT
    -Unblinded to treating clinicians but masked for paeds to assess neuro impairment
    -Babies included 26-32/40 with AC <10th and raised UAPI
    -3 branches with three different delivery strategies (CTG reduced STV, early DV changes, late DV changes)
  3. Primary outcomes
    -Survival without CP or neurosensory deficit at 2 yrs
  4. Secondary outomes
    -Composite measure of fetal death or postnatal death or severe morbidity
43
Q

Discuss the results of the TRUFFLE study
-Number included in study (1)
-Primary outcome results (3)
-Recommendation (2)

A
  1. Number included in the study
    -500 women randomised with FU data for 400 infants
  2. Primary outcome results
    -No differences in survival without neuro-impairment between the three groups
    -More deaths in late stage DV group but of those who survived more had normal neurological outcomes. (CTG 15% impaired, Early DV 9% impaired Late DV 5% impaired p = 0.004)
    -No significant difference in death rates between groups
  3. Recommendations
    -Base delivery time on Late stage DV changes
    -Deliver on CTG if STV <2.6 or 3ms depending on gestation
44
Q

Discuss the DIGITAT trial
-Aim (1)
-Study design (3)
-Primary outcomes (1)
-Secondary outcomes (3)

A
  1. Aim
    To compare IOL with EM for IUGR near term
  2. Study design
    -Multicentre RCT, not blinded
    -Included women >36/40 with suspected IUGR
    -Randomised to EM vs IOL
  3. Primary outcome
    -Composite measure of adverse neonatal outcomes
  4. Secondary outcomes
    -Mode of delivery
    -Length of stay in the neonatal unit
    -Maternal morbidity (PET, PPH, gHTN)
45
Q

Discuss the results of the DIGITAT study
-Number included
-Primary outcome results
-Secondary outcome results

A
  1. Number in study
    n = 650
    50% of the EM group were also induced
  2. Primary outcomes
    -No difference between groups for neonatal adverse outcomes 5.3 vs 6.1%
  3. Secondary outcomes
    -No difference in MOD between groups
    -No difference in NICU admission between the groups
    -Significantly more babies <3rd centile in the EM group cf the IOL group 31% vs 12%
46
Q

Discuss management of SGA according to NZ guidelines
-SGA up to 36+6
-SGA passed 37
-Timing of delivery

A
  1. SGA up to 36+6
    -USS every 2 weeks
    -Clinical review every 2 weeks
  2. SGA from 37/40
    -Consider weekly LV + D
    -Weekly clinical review
    -Aim birth at 40/40 and not before 39/40
47
Q

Discuss management of Early onset IUGR by NZ guidelines (4)

A

-At least weekly USS for LV + D
-Weekly CTG
-USS every 2 weeks for growth
-If AEDF or REDF then admit for birth planning (Deliver at 34/40 otherwise base delivery on DV)

48
Q
A

RANZCOG 2024 - Antenatal (12 decks)

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