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Pregnancy and Parturition > Regulation and Assessment of Fetal Growth > Flashcards

Regulation and Assessment of Fetal Growth Flashcards

1
Q

Why is fetal growth so important to track?

A

fetus’s that are less than the 3rd percentile in growth for gestation age have a very high risk for intrauterine death (still born, miscarriage)

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2
Q

What factors help regulate fetal growth?

A
  • genetics
  • endocrinology
  • environment
  • placentation

However it is not perfectly understood how growth is regulated in the fetus

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3
Q

Maternal and intrauterine environment contribute to about 60% of fetal weight. Fetus genotype is account for 15%, the maternal genome 20% and the Y chromosome only 2%.

Why does the maternal genome contribute more significantly than the paternal genome in regards to fetal growth?

A

Fetus needs to maintain appropriate size for mores pelvis and birthing canal for delivery hence the disproportionate parental genetic distribution

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4
Q

What are the genetic factors that contribute to fetal growth?

A
  1. maternal vs paternal genome
    - maternal more heavily contributed
  2. ethnic influences
    - customised growth charts
  3. Chromosomal abnormalities
    - aneuploidy
    -uniparental disomy
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5
Q

How does the endocrine system contribute to regulating fetal growth?

A
  1. Thyroid
    - both hyper and hypo thyroidism can contribute
  2. Pituitary
    - GH/TSH/prolactin
  3. Growth hormone
    - lower growth hormone leads to reduce IGF-1
  4. Insulin/IGF/IGF-BP
    - particularly IGF binding proteins (IGF-BP)
    - increased IGF-BP then there is less freely available IGF
    - IGF-BP1 increases with excess maternal inflammation and malnutrition
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6
Q

How does the environment contribute to fetal growth?

A
  1. uterine size (dictated by maternal genome)
    - fibroids, multiple gestation and malformation all take up space within the uterus which could obstruct the room needed for fetus to grow
  2. nutrition
    - pre-pregnancy and pregnancy
  3. Altitude
    - at higher altitudes there is reduced O2 binding to haemoglobin and the fetus will not recieve as much oxygen
  4. Drugs
    - therapeutic (ACE, anticonvulsants)
    - social (smoking, cocaine, alcohol)
  5. Infection
    - viral (Covid, CMV, HIV)
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7
Q

How does placentation contribute to fetal growth?

A
  1. primary (placenta damage)
  2. secondary (irregular placentation secondary to other pathologies):
    - SLE
    - diabetes
    - hypetension
    - lupus
    - nephropathies
    All cause abnormal vascularisation of the placenta
    - inflammation resulting in disordered placentation from endotheliopathy/vasculopathy
    - causes oxidative stress
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8
Q

The placenta is key for transporting nutrients across to the fetus. If this placenta is damaged, inflamed or scarred how does this affect fetal growth?

A

there is a decreased surface area that occurs lowering the effect of transportation across the placenta

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9
Q

What are the 3 kinds of feta growth abnormalities?

A
  1. macrosomia
    - larger than the 90th percentile for gestational age
  2. small for gestational age (SGA)
    - fetus under the 10th percentile for gestational age
    - these babies are small but are still healthy
  3. fetal growth restriction
    - asymmetric
    - symmetric
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10
Q

What is the difference between asymmetric and symmetric fetal growth restriction and what parameters are used to measure FGR?

A

parameteres:
- head circumference
- abdominal circumference
- femur length

asymmetrical FGR
- if one or two of the 3 parameters are measuring smaller for gestation age

symmetrical FGR
- all thee parameters measure small for gestational age

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11
Q

Asymmetrical FGR is more common and usually if left untreated will become symmetrical FGR. Why does this occur?

A

usually abdominal circumference is the first to decrease in size due to fetus malnourishment with head circumference last to decrease in size
- this is due to the brain being the most valuable organ and all of the sparse nourishment the fetus receives the brain takes it

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12
Q

Why is the abdominal circumference usually the first to decrease in size in FGR?

A

Due to malnourishment the fetus will use up the glycogen stores in the liver and covert to glucose for nutrition.

Long term use of glycogen stores causes the liver to become smaller and therefore the abdominal circumference decreases in size.

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13
Q

What is the broad definition of FGR?

A

an estimated fetal weight or abdominal circumference less that the 10th percentile for gestational age

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14
Q

What is the definition for severe FGR?

A

an estimated fetal weight or abdominal circumference less than the 3rd percentile for gestational age

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15
Q

What is the definition of FGR for the College of ObGyn?

A

AC or EFW less than 10th percentile for gestational age

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16
Q

What is the definitional of FGR for International society of ObGyn?

A

EARLY (less than 32 weeks)
- AC or EFW less than 3rd percentile for gestational age or umbilical artery absent end diastolic flow
OR
- AC or EFW less than 10th percentile for gestational age

combined with one of the following:
- uterine artery pulsatility index above the 95th percentile
- umbilical artery pulsatility index above the 95th percentile

LATE (at or after 32 weeks)
AC or EFW less than the 3rd percentile for gestational age
OR any two of the following:
- AC or EFW less than 10th percentile for GA
- AC/EFW crossing centiles more than 2 quartiles on growth centiles
- cerebroplacental ratio less than the 5th percentile or umbilical artery pulsatility index above the 95th percentile

17
Q

FGR/ intrauterine growth restriction aetiology is caused by:

A

fetal anomaly
- chromosomal 5%
- structural 7% (congenital heart/ kidney disease)

infection 5%

environment 10% (smoking, drugs, alcohol, nutrition, physical activity)

placental (majority of cases)

18
Q

FGR percentage by aneuploidy status compared to normal chromosomal numbers

A

normal chromosome amount
5-7% have FGR

trisomy’s
50% of trisomy fetuses have FGR

19
Q

What are the placentation causes of FGR?

A
  1. idiopathic (cause unknown)
  2. hypertensive disorders
    - pre-eclampsia
    - chronic hypertension
  3. antiphospholipid syndrome (APLS)
    - greater risk for developng blood clots
  4. Thrombophilias
    - cause blood clots in microvasculature
    - reduced gas/nutrient exchange
  5. Other medical disorder
    - diabetes
    - renal disorders
  6. Being male
    - Y chromosome is not as efficient as second X chromosome
  • blood clots cause lack of transport across the placenta due to specific area not working due to lack of blood flow
20
Q

What is the normal pathology of blood vessels in the placenta?

A

high capacitance
low resistance to increase blood flow

21
Q

In pre-eclampsia, the vessels in the placenta are altered. What changes that affects the placentas function?

A

high resistance in vessels

low capacitance
- poor perfusion
- reduced nutrient/gas-exchange
- inflammation
- vascular shear stress/ endothelial dysfunction

22
Q

Why is umbilical artery waveforms measured by doppler used as a factor to determine FGR?

A

umbilical artery goes from baby back to placenta

umbilical artery waveforms help identify pulsitility index.

If placenta is dysfunctional there is an increased resistance to blood flow back to placenta

23
Q

What does reversed diastolic flow on umbilical artery waveforms display?

A

demonstrates that there is reversal of umbilical cord flow
- there is back flow meaning that deoxygenated blood is going back to the fetus due to resistance in cord and/or placenta
- causes the babys heart to over work to overcome the resistance

24
Q

With doppler umbilical artery waveforms increased resistance is seen first then followed by absent end diastolic flow then reversal end diastolic flow. What happens to the fetus during the decreasing placental function?

A

increased resistance:
- reduced fetal growth

if increased resistance continues:
- fetal hypoxia

absent end diastolic flow:
- fetal acidaemia (acidosis)
- decrease in pH due to lack of oxygen and increased CO2

reversed end diastolic flow:
- severe fetal acidosis and demise

25
Q

What are the long term consequences of FGR?

A

FGR results in fetal adaptations like:
- organ adaptations
- cardiovascular/endothelial dysfunction
- altered neurodevelopment and possible neuro-behavioural adversity

26
Q

What is the relationship between SGA and FGR

A

most SGA fetuses are not FGR fetuses

a significant number of inter-uterine growth restriction fetuses have a birth weight within the normal range

27
Q

How is FGR detected

A
  1. clinical examination (not as accurate as ultrasound assessment):
    - abdominal palpation
    - symphyisiofundal (SFH) height
    +50-75% detection rate
    +30% specificity
    - maternal subjective assessment
  2. Ultrasound assessment
    - fetal biometry
    - doppler studies
    + umbilical artery
    + uterine artery
    - amniotic fluid assessment
28
Q

What is fetal biometry measured in ultrasound assessment for FGR detection?

A

AC = abdominal circumference
HC = head circumference
BPD = biparietal diameter
FL = femur length

29
Q

How is FGR managed

A

management depends on:
- severity of FGR
- onset of disease (early vs late)
- aetiology
- overall ‘trend’
- doppler and amniotic fluid findings

30
Q

What diagnostic tools are used to differentiate between IUGR and SGA?

A

doppler ultrasound of umbilical artery pulsitility index and measurement of amniotic fluid

31
Q

If fetuses around to be under the 10th percentile for weight what diagnostic testing should be offered as the first step?

A

anatomical surveying and karyotyping

32
Q

How is fetal/maternal surveillance and delivery planning clinically determined?

A

should be tailored to gestation and severity

Pregnancy and Parturition (10 decks)

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