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Fetus > Normal and disordered fetal growth > Flashcards

Normal and disordered fetal growth Flashcards

1
Q

How do you know if a baby is under or overgrown

A

Assess size at particular point of gestation, compare to spectrum of normality for that time point.
Normal = between 10th and 90th percentile

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2
Q

Define SGA

A

Small for gestational age

Fetus <10th weight percentile for age

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3
Q

Define IUGR

A

Intrauterine growth restriction

Fetus unable to achieve genetically predetermined size

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4
Q

Define LBW

A

Low birth weight
Less than 2500g regardless of gestational age
Can be due to SGA or prematurity

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5
Q

What are the classes of SGA fetuses

A

Normal small fetus- no structural abnormality, normal umbilical artery. Not at risk, no special care needed
Abnormal small fetus- chromosomal or structural abnormality
Growth restricted fetus- results from placental dysfunction

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6
Q

What is the risk of assessing for SGA

A

Many normal/healthy SGA fetuses are subjected to high risk protocols and potentially iatrogenic prematurity

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7
Q

What is FGR

A

Fetal growth restriction, can be symmetrical or asymmetrical

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8
Q

What is symmetrical FGR

A

Head and body proportionately small
Fetal insult during early development
Affected cell growth and hyperplasia

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9
Q

What is asymmetrical FGR

A

Fetal brain disproportionately small large compared to liver (normal ratio >3, asymmetrical >6)
Fetal insult during later development
Placental problems common

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10
Q

What is skeletal dysplasia

A

Distinct growth patterns due to differential impacts on axial and peripheral skeletal growth

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11
Q

What are the classes of causes of IUGR

A

Intrinsic, Extrinsic

Maternal, fetal, placental

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12
Q

What are the intrinsic causes of IUGR

A

Chromosomal abberations
Congenital structural defects
Genetic constitution

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13
Q

What are the maternal causes of IUGR

A

Infection eg. toxoplasmosis, malaria, rubella, cytomegalovirus
Chronic disease eg. hypertension, renal disease, advanced diabetes, haemoglobinopathies
Preeclampsia
High altitude
Malnutrition
Drugs

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14
Q

What are the fetal causes of IUGR

A

Multiple pregnancy
Infection
Extra-uterine pregnancy

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15
Q

What are the placental causes of IUGR

A 
Uteroplacental insufficiency
Defective invasion/placentation
Lateral insertion of cord
Reduced blood flow to placental bed eg. preeclampsia
Vascular anomalies
Decreased functioning capacity
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16
Q

What is the underlying mechanism of IUGR

A 
Insufficient gas exchange and nutrient delivery to fetus:
Decreased O2 carrying capacity (cyanotic heart disease, smoking, hameoglobinopathy)
Dysfunctional O2 delivery system (diabetes with vascular disease, hypertension, autoimmune conditions)
Placental damage (smoking, thrombophilia)
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17
Q

How do we know the intrauterine environment is important in fetal development

A

Recipient mother is more important for fetal growth than egg donor in embryo transfer

18
Q

What is the role of maternal nutrition in fetal development

A

Undernutrition reduces placental and fetal growth

19
Q

When is fetal growth most vulnerable to maternal dietary deficiencies

A

During the peri-implantation stage and periods of rapid placental development

20
Q

What is the molecular mechanism of fetal programming

A

Nutritional insult during development leaves memory by altering epigenetic state of fetal genome
Epigenetic alterations in early embryos can be carried forward to later developmental stages
Either DNA methylation or histone modification- methylation or acetylation

21
Q

What are the 3 main placental function

A

Transport
Metabolism
Endocrine

22
Q

How are nutrients transported across the placenta

A

Glucose- facilitated diffusion, hexose transporters

Amino acids- active transport

23
Q

Which antibodies are transported across the placenta

A

IgG

24
Q

How is bilirubin transported across the placenta

A

Conjugated form from mother is poortly transported

Unconjugated from fetus crosses easily

25
Q

What are the perinatal implications of IUGR

A

Increased morbidity/mortality- iatrogenic prematurity, fetal compromise in labour, need for induction or caesarian
Stillbirth- due to prematurity, asphyxia or congenital malformations

26
Q

What are the risks of prematurity

A 
Necrotising enterocolitis
Thromocytopenia
Temperature instability
Respiratory distress syndrome
Renal failure
Metabolic problems
27
Q

What is the thrifty phenotype hypothesis

A

Metabolically deprived fetus becomes metabolically programmed for insulin resistance and impaired glucose metabolism
Strong association between FGR and prevalence of type 2 diabetes

28
Q

How is IUGR managed

A

Identify those at risk, diagnosis, surveillance until risk of in utero demise exceeds risk of delivery

29
Q

How is IUGR diagnosed

A

Presence of risk factors
Clinical- serial maternal weight, symphysio-fundal height assessment
Ultrasound- inadequate fetal growth, reduced amniotic fluid index, placental calcification, fetal biometry
Customised fundal height charts

30
Q

What are the advantages of customised fundal height charts

A

Improved sensitivity

Takes into account: maternal height, weight, parity, ethnicity

31
Q

What does IUGR surveillance entail

A 
Serial scans
Non-stress test
Amniotic fluid assessment
Umbilical doppler
Biophysical profile assessment
32
Q

How are uteroplacental dopplers used in IUGR

A

Uterine- High resistivity index, notch in pulmonary embolism. High false positive, low positive predictive value
Umbilical arteries- Increased impedance to flow in FGR. Absence then reversal and end diastolic flow. Increased incidence of lethal abnormalities. High risk pregnancies should have UA dopplers

33
Q

How are fetal dopplers used in IUGR

A

Pulsatility index, ductus venosus and short-term variation important indicators for timing of delivery before 32 weeks
Delivery if any parameter becomes consistently abnormal

34
Q

What ancillary invasive tests are done in IUGR

A

Fetal karyotyping
Fetal blood sampling
Amniocentesis for lecithin-sphingomyelin ratios

35
Q

How is IUGR diagnosed neonatally

A

Low ponderal index
Low subcutaneous fat
Hypoglycaemia, hyperbilirubinaemia, necrotising enterocolitis, hyperviscosity syndrome

36
Q

How is IUGR prevented

A

Largely unpreventable by some evidence of benefit for LDA and miniheparin, reducing maternal smoking, antibiotics to prevent UTIs, antimalarial prophylaxis

37
Q

Define LGA

A

Large for gestational age

Fetal size >90th percentile for that gestation

38
Q

Define macrosomia

A

Birth weight >4000g regardless of gestational age

39
Q

Timeline for assessing IUGR (detailed)

A

Booking assessment during 1st trimester
If 3+ minor risk factors or 1 major risk factor the reassess at 20 weeks using PAPP-A (<0.4) or MOM, fetal echogenic bowel
If 3 or more minor risk factors uterine artery doppler at 20-24 weeks. If normal, assessment of fetal size and umbilical artery doppler in third trimester
If UA doppler abnormal major risk factor then serial assessment of fetal size and umbilical artery doppler from 16-18 weeeks
Reassess during 3rd trimester

40
Q

What are the risk factors for macrosomia

A 
maternal hyperglycaemia
Previous macrosomic infant
Pre-pregnancy obesity
Male fetus
Post-term gestation
Parental height + race
Maternal age <20 years
41
Q

What are the problems of fetal overgrowth

A

Maternal diabetes
Fetal demise
Birth trauma eg. shoulder dystocia
Neonatal hypoglycaemia

Fetus (18 decks)

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