fetal wellbeing

Question 1

Small for gestational age definition

Answer 1

• infant with birthweight less than the 10th birth weight centile
• a fetus with an estimated fetal weight (EFW) less than the 10th customised centile for gestation.

Question 2

Fetal growth restriction

Answer 2

• SGA + abnormal dopplers OR EFW <3rd

* EFW or AC crossing centiles / major discrepancy between HC and AC

Question 3

What are the major risk factors that recommend serial growth scans identified at booking

Answer 3

• a history of a previous SGA or stillborn infant
• maternal age >40
• maternal or paternal history of being SGA at birth
• smoking >10 cigarettes daily
• using cocaine
• Maternal diseases associated with increased risk (e.g. chronic hypertension,
renal disease, diabetes with vascular disease, anti-phospholipid syndrome)

Question 4

What complications in the current pregnancy are recommended to have a plan for serial growth scans in the third trimester

Answer 4

• heavy early pregnancy bleeding
• fetal echogenic bowel
• Preeclampsia
• Severe pregnancy-induced hypertension
• Unexplained ante-partum haemorrhage or abruption
• Low gestational weight gain
• Low PAPP-A

Question 5

Who should get an Uterine artery Doppler studies at 20-24 weeks to help diagnose severe SGA?

Answer 5

• previous early SGA with delivery <34 weeks
• anti-phospholipid syndrome
• severe chronic hypertension
• Maternal renal disease
• autoimmune condition

Question 6

What is the significance of raised uterine artery doppler at 20-24 weeks?

Answer 6

Woman with very abnormal uterine artery Doppler studies have an approximately 60% risk of developing SGA or preeclampsia requiring delivery <34 weeks should have regular scans and maternal surveillance

Question 7

Prevention of SGA

Answer 7

≤ 16 weeks’ gestation low dose aspirin (100 mg per day) may be considered as this reduces the risk of SGA, especially in women who also have risk factors for preeclampsia, such as those with underlying medical disorders

Smoking cessation

Question 8

If no risk factors, who gets growth scans?

Answer 8

• A growth scan is recommended if SFH is reducing centiles (e.g. >30%) or is < 10th %
• A growth scan is not recommended in women where SFH is tracking along or above the 90th centile if GDM has been excluded and there is no clinical concern re polyhydramnios.

Question 9

what is the risk of SGA infant if previous SGA

Answer 9

three-fold increase in risk of SGA

Question 10

Underlying Medical Conditions if associated with SGA require additional monitoring eg

Answer 10

Serial growth scans (3-4 weekly) are recommended with more frequent growth scans (2-3
weekly) if sup-optimal growth is suspected.

Question 11

Consequence of smoking on SGA

Answer 11

Women who become smoke-free by 15 weeks have no increase in risk of SGA compared with nonsmokers

Question 12

Obese Women

how to perform SGA monitoring

Answer 12

plan for growth scans is recommended with a
BMI of >35 is not possible to assess fetal growth clinically, growth scans may be considered at 30-32
weeks’ and at 36-38 weeks’ to enable serial assessment of fetal growth If a single scan is performed – better at 36-38 weeks (not allow trends)
More frequent / earlier scans are indicated if additional risk factors are present.

Question 13

how does PAPP A affect SGA

Answer 13

Low PAPP-A is associate with increased SGA and PET - Low dose aspirin if low PAPP-A (<0.2 MoM) if less then 20 weeks

Question 14

Management of SGA

Answer 14

• advice about fetal movements.
• Monitor for PET / HTN as can be the initial presenting complaint (In nulliparous women about 25% of SGA babies are born to women with hypertensive complications (preeclampsia, gestational hypertension, chronic hypertension)
• regular monitoring of BP and urinalysis performed at each clinical visit

Question 15

Management of SGA with abnormal UA Doppler -

Answer 15

Plan for twice-weekly fetal and maternal surveillance as an outpatient, Association with maternal hypertension (PET) is common

Question 16

SGA with normal UA Doppler –

Answer 16

2/3 SGA have normal dopplers
¾ of these pregnancies with have histological evidence of abnormal uteroplacental perfusion
Increased risk if morbidity if also growth restricted – if SGA and growth restricted they should be delivered by 38 weeks

Question 17

SGA with abnormal MCA/ CRP –

Answer 17

Twice weekly surveillance, including
• clinical review
• CTG
• least weekly umbilical artery and MCA Doppler studies
• amniotic fluid volume (single deepest vertical pool of amniotic fluid)
• Scans for growth every two to three weeks
• Document the management plan in the clinical record.
• Deliver by 38 weeks

Question 18

What are the investigations for early onset IUGR

Answer 18

If severe SGA is identified at the anatomy scan then referral to fetal medicine and uterine artery dopplers is indicated
Karyotyping is offered if SGA identified before 23 weeks or is there are associated structural abnormalities
CMV and toxoplasmosis is indicated
Syphilis and Malaria should be tested in at risk populations

Question 19

Delivery based on MCA?

What does the MCA represent?

Answer 19

Preterm - do not deliver based on MCA

Term (37 weeks) deliver if abn MCA
bn MCA is a sign of brain sparing affect of chronic hypoxia - it is an early sign of fetal hypoxia

Moderative predictive value for acidaemia at birth (increased EMLSCDS and neonatal admission) in term infants

Question 20

What is the DV?

When to measure?

When to deliver?

Answer 20

Used as a surveillance in preterm infants with abnormal umbilical artery doppler to time delivery
Moderate predictive value for acidosis and adverse outcomes
DV flow velocity reflects atrial pressure volume changes over the cardiac cycle
Retrograde a wave signifies overt fetal cardiac compromise

Question 21

How to diagnose hydrops

+ what are the USS associations

Answer 21

2 of the following 4

1. Ascites
2. Pleural effusion
3. Pericardial effusion more then 2mm - increasing is a bad sign
4. Skin oedema (chest / scalp more then 5mm)

Associated with polyhydramnios (SDP over 8 or AFI > 24)
Placental thickening due to intravillous oedema - more then 4cm in T2 or 6cm in T3
Note if poly can obscure thickening of placenta

Question 22

What are the maternal effects of having a hydropic baby?

Answer 22

Large for dates
Theca lutein cysts (increased hcg – unclear pathology - ? increase villous oedema)
PET (mirror syndrome)
Generalised maternal oedema often with pulmonary involvement
Can occur at any time – presenting with rapid weight gain, increasing peripheral oedema, SOB
Maternal haematocrit is low (in contrast to PET)
Rate IUD 50%
Severe polyhydramnios – maternal respiratory symptoms

Question 23

What are theca lutein cysts?

Answer 23

Theca lutein cysts (increased hcg – unclear pathology - ? increase villous oedema)
Functional ovarian cysts, typically bilateral and multiple
Highest in GTD , also GDM pregnancies and hydropic babies
More likely in PCOS woman
Ovaries can be 10-15cm, pressure symptoms, 30% of woman with these will be hirsute or virilized

They are thought to originate due to excessive amounts of circulating gonadotrophins such as beta-hCG. Hyperplasia of the theca interna cells is the predominant characteristic on histology. The ovarian parenchyma is often markedly edematous and frequently contains foci of luteinized stromal cells.

Question 24

Causes of fetal anaemia

Answer 24

Infection - parvovirus B12
Red cell alloimmunisation
Fetal maternal haemorrhage
hematological disorder eg thalassaemia

rarely
red cell production disorders
Enzymopathies
structural red cell abnormalities (hereditary spherocytosis)
myeloproliferative disorders (leukaemia)

Question 25

Work up for hydrops

Answer 25

MFM referral
Indirect coombs test for alloimmunisation
Detailed anatomy
Fetal ECHO
Maternal Hb - if low genetic screen thalassaemias
MCA doppler velocimetry for anaemia
Amnio for karyotype and for infection screen, chromosomal microarray
Kleihauer

Question 26

Ddx hydrops

Answer 26

Alloimmunisation 
Aneuploidy 
T1 50% T2 20% turners post common
Cardiovascular 20% 
- structural
- arrhythmia
- cardiomyopathy
Hematological  10%
- haemoglobinopathies
- enzyme or membrane disorders, erythrocyte aplasia 
FHM
Infection 
- parvovirus B19, syph, CMV, EBV, Toxo, rubella, enterovirus varicella, 
Thoracic abnormalities 6% 
- pulmonary sequestration, cystic adenomatoid malformation, diaphragmatic hernia
Lymphatic abnormalities
Placenta/ twin complications
Kidney and urinary tract abnormalties
Syndromic
Weird and wonderful

Question 27

Mortality rate of hydrops

Answer 27

chance of live birth after prenatal dx 40%

Neonatal survival 50%

Question 28

What is mirror syndrome
How is it different to PET

What tests can be done

Answer 28

associated with fetal hydrops and maternal oedema
associated with Rh D alloimmunisation, TTTS, Placental chorioangioma, fetal cystic hygroma, infections, cardiac anomalies, renal / bladder anomalies

90% oedema, 60% HTN, 40% proteinuria,
Similar to PET but haemodilution (not concentration like PET)
Elevated sfms-like kinase 1
Decreased placental growth factor
elevated vascular endothelial growth factor receptor 1

Generally prompt delivery indicated

Question 29

what doppler detects anaemia

Answer 29

MCA peak systolic volume PSV

not just PI

Question 30

why is alloimmunisation actually pretty uncommon

1%

Answer 30

1. low prevalence of incompatible antigens
2. Insufficient transplacental passage
3. Maternal fetal ABO incompatability so rapidly clearance of antigens before an immune response
4. variable antigenicity
5. variable immune response to the antigen

Question 31

What antibodies cause severe HDFN

Answer 31

Anti D,
Anti c
Level >7.5 but <20 correlates with a moderate risk of HDFN – referral once >7.5
If Anti E is also present then referral at lower titres maybe indicated
Anti K
Referral once detected as severe fetal anaemia can occur at 1:8

Question 32

Antibodies that do NOT cause alloimmunisation

Answer 32

Lewis antibodies Le (a) Le (b) and I antibodies – mainly IgM and not expressed on fetal red cells

Also Duffy group B – fy(b)

Question 33

What is the indirect coombs test

Answer 33

Indirect coombs test

Patients plasma + Red cells with known antigens + coombs reagent (antibodies againt human antigens)

Agglutination = positive test

Use Indirect coombs test for pretransfusion testing and blood type cross matching

Question 34

What to consider with kell antibodies

Answer 34

Anti Kell antibodies cause hemolysis AND suppress erythropoieses by destroying the RBC progenitor cells in the BM

Severe anaemia can occur at low titres

Not for titre measurement – does have MCA PSV from 16 weeks

Question 35

Anti D
What gene
Complication rate
How much blood results is needed for sensitisation 
What si the ethnic variation

Answer 35

D is the most immunogenic
Complicates 0.5-0.9% pregnancies
0.1mls of Rh postive blood can cause sensitization
Responsible genes chromosome 1 RHD and RHCE
A single transion of + blood to a negative person have a 50% of forning anti D IgG
Ethnic variation in prevalence
85% Americas Rh +, 90% native americas, 93% African Americans, 99% Asians
Maternal alloimmunisation by exposure to anti D by incompatible blood transion or needle sharing

Question 36

How to prevent anti D sensitisation

Answer 36

Recognise and treat sensitizing events
Within 72 hours but can give up to 9-10 days
6 weekly
Management
Blood group antibody screen at blooking and 28 weeks
Antenatal prophylaxis 28 + 34 weeks 625 IUI
Indicated prophylaxis
First trimester
CVS
Miscarriage
Termiantion
Ectopc
Not enough evidence for threatened miscarriage before 12 weeks
Second and third trimester
APH
Amniocentesis. Cordocentesis
ECV (successful ir not)
Abdo trauma or other suspective intrauterine bleeding
Directed prophylaxis in the Rh + neonate
Can assess volume after sensitising event
Kleihauer, flow cytometry
Give additional anti D if needed

Question 37

Approach to a sensitised pregnancy

Answer 37

Maternal antibody titres and quantification
Anti D, c, K monthly until 28 weeks then every 2 weeks
If other antibodies consider paternal testing

Assess fetal risk
- paternal testing
Fathers blood phenotype and genotype
If father is Rh + but hereozygous 50% of children with be RH neg
NIPT
Assess fetal genotype – if doesnt have Antigen then not as risk
Indicated if father is heterozygous
Amniocentesis and PCR of amniocytes
CVS is not used may worsen alloimmunisation and increased FMH
Maternal hx
Monitoring antibody
Quantitation is more reliable then titre
Referral 1:16/32 = 4-6 quant

Refer to MFM 
Hx of haemolytic disease  
High titres, abnormal USS 
Critical titre reached 
MCA PSV approaching / 1.5 MoM

Question 38

Management of an at risk pregnancy

• high titres
• anti Kell

Answer 38

Fetal monitoring

MCA PSV (peak systolic velocity)
Increased velocity due to creased cardiac output, vasodilation of the brain, decreased blood viscosity
Technique
Resting fetus, Circle of Willis imaged in axial image using colour doppler, Entire length of MCA, Close to origin of internal carotid artery

Gestation dependent  
Measure from 18-20 weeks, to 36 weeks  
Not as efficacious after 36 weeks  
Levels <1.5Mom = 100% not anaemic 
Measure 2 weekly 
Levels >1.5 Mom = 65% anaemic 12% false +  
Repeat in 24 hours – if the same then FBS +/- transfuse  
After IUT MCA maybe unreliable  
Liver length is a helpful adjunct  
Assess for signs of hydrops

Question 39

incidence and definition of polyhydramnios

Answer 39

1-2% o pregnancy
SDP > or=8
AFI >24

Question 40

Ddx for polyhydramnios

Answer 40

Causes - Likelihood of finding a cause is related to severity of polyhydramnios

Idiopathic 40%
Fetal structural anomaly/anomalies
Most commonly when swallow was affected
GI obstruction – duodenal, esophageal, intestinal
Neuromuscular disorders – anencephaly
Secondary obstruction eg massive unilateral dysplastic kidneys

Fetal chromosomal abnormality (eg, Trisomy 18)
IUGR + Poly think T18
10-20% of severe poly has a chromosomal condition

High fetal cardiac output state (eg, any condition resulting in anemia)
Anaemia from alloimmunization, haemolysis

Twin-twin transfusion syndrome
Maternal diabetes mellitus // lithium use / substance us

Fetal neuromuscular disorders
Fetal infection (eg, parvovirus)
Fetal Bartter syndrome
Rare autosomal renal tubular disorder

Question 41

What does having poly increase the risk of ?

Answer 41

maternal respiratory compromise 
PTB PPROM PTL 
Malposition
Macrosomia
Umbilical cord prolapse
abruption (with ROM) 
Longer second stage
POst partum atony

perinatal mortality 5.5X higher
Idiopathic - increases the risk of low 5 min apgar, TTN, needing resus, NICU, hypoglycemia, structural abnormalities, jaundice
Long tern neurological disorders , developmental delay,

Question 42

What is the management only poly diagnosed?

Answer 42

Detailed family hx
Genetic testing for severe polyhydramions
GTT
TORCH if other signs of fetal infection
Review blood group and antibody status
Anatomy - (with a normal anatoym scan and severe poly risk of a major malformation 11%)

Question 43

Are there any treatments for polyhydramnios

Answer 43

The aim is to relieve maternal symptoms and to reduce the risk of preterm labour, by reducing uterine stretch.

Amnioreduction

Studies have shown that this can prolong gestation and improve perinatal survival. However, it may need to be repeated and can result in stimulation of preterm labour, or abruption due to the rapid reduction in intrauterine pressure.

Indomethacin

This may work by enhancing fetal renal reabsorption of water and sodium and, hence, reducing the amount of urine produced by the fetal kidneys.

Indomethacin has been reported to be associated with premature closure of the ductus arteriosus, cerebral vasoconstriction, and impaired renal function in the neonatal period. For these reasons, its use is usually discontinued at 32 weeks of gestation. The use of indomethacin is contraindicated in twin-to-twin transfusion syndrome as it may have adverse effects on the oliguric donor twin.