Foetal Growth Restriction and Large for Dates Flashcards
Definition of small-for-gestational age
An infant born with a birth weight less than the 10th centile. Use centiles customised for maternal characteristics (maternal height, weight, parity, ethnicity) as well as gestational age at delivery.
Definition of foetal growth restriction
Implies a pathological restriction of the genetic growth potential. This may manifest evidence of foetal compromise (abnormal Doppler studies, reduced liquor volume.)
Definition of low brith weight
Refers to an infant with a birth weight <2.5 Kg
Maternal causes of SGA
- HTN, T2DM, drugs (smoking, cocaine use), renal disease, thrombophilia, advanced maternal age (age> 40), nulliparity, daily vigorous exercise, pemphigoid gestionis
- Previous pregnancy Hx: Previous SGA baby, previous stillbirth, previous pre-eclampsia, high pregnancy interval
- Current pregnancy complications/developments: Pre-eclampsia, severe PIH, low maternal weight gain, placental abruption
Foetal factors with cause SGA
Chromosomal abnormalities, infection (CMV, rubella), multiple pregnancy
Other causes of SGA (not maternal or foetal)
Placental insufficiency:
* Reduced uteroplacental perfusion due to: inadequate trophoblast invasion (commonest cause in developed world- similar to PET), sickle cell disease, multiple gestation
* Reduced fetoplacental perfusion: Sigle umbilical artery, Twin-to-twin transfusion syndrome
Incidence of SGA
3-5% of pregnancies
How can SGA be classified
- Symmetrical: Usually due to factors that directly impair foetal growth (chromosomal disorders, foetal infections)- Typically early onset, head and body are proportionally small
- Asymmetrical: Associated with uteroplacental insufficiency leading to reduced oxygen transfer to foetus and reduced CO2 removal- Typically later onset, abdominal circumference disproportionately smaller than the head
What is the pathophysiology of asymmetrical SGA
- When the foetus is hypoxic, more of the well-oxygenated blood will bypass the liver via the ductus venosus, meaning the liver receives very little oxygenated blood
- Fall in pO2 and rise in pCO2 in the foetus induces chemoreceptor response in foetal carotid bodies- results in vasodilation in the foetal brain, myocardium and vasoconstriction in kidneys, splanchnic vessels, limbs and subcut tissue
- This results in an asymmetrical foetus with relative brain sparing and reduced abdominal girth and skin thickness
- Vasoconstriction in the foetal kidneys results in impaired urine production and oligohydramnios
- Chronic foetal hypoxia in FGR can lead to foetal acidaemia (respiratory and metabolic ) which can lead to intrauterine death if prolonged (risk of profound asphyxia is increased in labour due to compromise of uteroplacental circulation.
Signs of FGR
Reduced amniotic fluid volume, abnormal doppler studies, reduced foetal movements, abnormal CTGs
Complications of FGR
Short term complications of FGR include:
* Foetal death or stillbirth
* Birth asphyxia
* Neonatal hypothermia and hypoglycaemia
Long-term complications include:
* Cardiovascular disease, particularly HTN
* T2DM, obesity, mood and behaviour problems
What are the major risk factors for FGR
HTN, T2DM, smoking, cocaine use, age > 40, daily vigorous exercise, previous SGA or stillbirth, PET, severe PIH, low maternal weight, CMV, rubella, placental insufficiency
How should women be monitored during the antenatal period for FGR
- All women should be assessed at booking for risk factors for an SGA foetus/ neonate to identify those who require increased surveillance
- Women who have a major risk factor should be referred for serial ultrasound measurement of foetal size and assessment of wellbeing with umbilical artery doppler from 26-28 weeks of pregnancy
- A low level of the first trimester marker PAPP-A should be considered a major risk factor for delivery of a SGA neonate
- Women who have three or more minor risk factors should be referred for uterine artery Doppler at 20-24 weeks gestation
- In women with an abnormal uterine artery Doppler at 20–24 weeks, subsequent normalisation of flow velocity indices is still associated with an increased risk of a SGA neonate. Should have serial USS measurement commencing at 26-28 weeks
- Women with a normal uterine artery Doppler do not require serial USS measurement unless they develop specific pregnancy complications, for example antepartum haemorrhage or hypertension
- Abdominal palpation has limited accuracy for the prediction of SGA neonates and should NOT be routinely performed for this purpose
- Serial measurement of SFH is recommended at each antenatal appointment from 24 weeks- improves prediction rates
How can SGA be diagnosed
- Women with a single SFH which plots below the 10th centile or serial measurements which demonstrate slow or static growth by crossing centiles should be referred for ultrasound measurement of fetal size
- Fetal abdominal circumference (AC) or estimated fetal weight (EFW) < 10th centile can be used to diagnose a SGA foetus.
What further investigations should be offered if there is suspected FGR
- Serological screening for congenital cytomegalovirus (CMV) and toxoplasmosis infection should be offered. Testing for syphilis and malaria should be considered in high risk populations
Summary of SGA management
Summary of SGA management
Investigations for SGA summary
