fetal growth restriction Flashcards
define small for gestational age *
birth weight <10th centile
define fetal growth restriction *
failure of teh fetus to achieve its predetermined growth potential for various reasons
define low birth weight, very low birth weightm extremely low *
less than 2.5kg at delivery
<1.5
<1
(very and extremely dont take into account gestational age - <1.5 might not be SGA etc if premature…)
what are the signs of early IUGR (intrauterine growth restriction) *
abnormal size and umbilical doppler (blood flow)
describe the relationship between low birth weight (LBW), fetal growth restriction, and preterm delivery*
most LBW babies are not growth restricted
many FGR babies are delivered prematurely to prevent still birth
they have closely associated pathologies
describe SGA *
statististical definition for weight at birth - below a subjective cemtile on charts of birth weight standards - usually 10th, 5th or 3rd
when choosing which centile, have to balance between sensitivity and specificity - 10th is sensitive and will capture all FGR babies but alos include those SGA (false +ves); all using the 3rd will be FGR but might miss some (false -ves) - specific
LGA is above 9th
when should you use the term FGR *
only when it is evident that growth has altered - growth is dynamic therefore can only be diagnosed over serial observations
FGR children are at more risk of morbidity and mortlity than SGA/LBW
consequences of FGR/IUGR *
most common factor in stillborn
increased risk of IUGR and intrauterine death insubsequent pregnancies
short term
- resp distress
- intraventricular haemorrhage
- sepsis - give AB to prevent
- hypoglycaemia - give dextrose drip to prevent
- necrotising enterocolitis - bowel ischemic
- jaundice with the weight loss
- electrolyte imbalance in initial stages
medium term
- respiratory problems
- developmental delay
- special needs schooling - learning difficulties
long term
- fetal programming - lead to adult problems
causes of SGA *
dating problem - when consistant growth and normal dopplers and amnio fluid
normal - growth may reduce in 2 weeks but continue to grow, normal dopplers and fluid
fetal problem - 5% - fetal abnormality eg chromosome/infection
placental insufficiency - 20% - reduction in AC/FL (because lost fat deposition in the liver), reduced liquor (because diverting blood to brain), deranged dopplers (reduced amniotic fluid because they wee less to conserve fluid)
disruption in substrate, blood flow or genetci factors can effect growth
maternal medical factors causing SGA and FGR *
•Chronic hypertension
Connective tissue disease
Severe chronic infection
Diabetes mellitus
Anaemia
Uterine abnormalities
Maternal malignancy
Pre-eclampsia
Thrombophilic defects
maternal behavioural factors causing SGA and FGR *
Smoking
Low booking weight (<50 kg)
Poor nutrition
Age <16 or >35 years at delivery
Alcohol
Drugs
High altitude
Social deprivation
placental factors causing SGA and FGR *
impared trophoblast invasion
Partial abruption or infarction
Chorioamnionitis
placental cysts
Placenta praevi
fetal factors causing SGA and FGR *
Multiple pregnancy
Structural abnormality
Chromosomal abnormalities
Intrauterine (congenital) infection
Inborn errors of metabolism
describe the development of the placenta *
10-12 weeks is the period of placentation
happens in 2 waves - 1st is primary implantation, 2nd occurs at 14-16wks and lasts for 4 weeks
rapid early growth prepares way for fetal growth
trophoblast cells use the same molecular mechanisms as tumours, but are highly regulated and controlled - any interruption = FGR
roles of the placenta *
maintain immunolgical distance between the placenta and the mother
special endocrine organ - produces protein peptides and steroid hormones and functions as a transient HPG axis
exchange nutrients, gases and metabolic waste products between maternal and fetal circulation
describe what causes an increase in the pressure in the system in pre-eclampsia*
normally the spiral arches in the blood vesslesl lose muscle so are wider (this remodelling is done by cytotrophoblast) - allow more blood and nutrients through
in PET - spiral arches are narrow = decreased blood flow and increased pressure because high resistance
PET therefore causes decreased nutrient supply to the placenta and fetus which can cause FGR
describe pre-eclampsia *
it is maternal hypertension and protienuria
hypertension disorders occur in 10% of pregnancies - ony 1-2% severe form, fetal syndrome (ie FGR without maternal complications) very rare
define pre-eclampsia *
multisystem disease that usually manifests as hypertension (so that they pump more blood to the placenta) and proteinuria (because capillaries leaky)
’’ gestational hypertension, BP >140/90, on 2 occaisions >/=4hrs apart and protein >0.3g/24hr (PCR>30) arising de novo in a normally normotensive women adn resolving completely by 6th post-partum week’’
- Mild140-149/90-99mmHg
- Moderate 150-159/100-109mmHg
- Severe ≥160/110mmHg
happens de novo
after 20th week and resolves by 6th post-partum week - people with high BP at 12weeks have chronic hypertension not pre-eclampsia
which fetuses need monitoring *
when women have a poor obs history - previous maternal hypertension, previous FGR, stillbirth, placental abruption
when concerns in index preg - abnormal serum biochem (PAPP-A <0.3MoM - marker for Down’s and placenta insufficiency - increased risk of pre-eclampsia/FGR), reduced SFH, maternal systemic disease (hypertension, renal, coagulation), antepartum haemorrhage, multiple pregnancy
what is the maternal history of someone whose fetus might have FGR *
Poor Obstetric History
Primips
Obese
Afro-Carribean / African
Strong Family History
Essential hypertension
Diabetes / Impaired Glucose Tolerance
Systemic vascular disease
Renal disease
Thrombophilias
what is the screening for at risk pregnancies *
at 24wks
PAPP-A <0.3MoM, POHx, PET/FGR
maternal systemic disease
uterine artery doppler 1st/2nd trimester - look at blood flow through the uterine arteries to identify high resistance flow
describe uterine artery doppler screening *
arteries narrow = increased resistance = increased BP to support circulation
see notching in poor uterine blood flow
4x increased risk of PET and FGR
what are the sequence of events in FGR *
uterine artery abnormality = more abnormality in spiral arch = higher resistance in umbilical artery - only evident when at least 60% of placental vascular bed is obliterated
baby tries to conserve energy so doesnt move
diverts blood to major organs - brain sparing
kidneys shut down = reduction in amniotic fluid
baby becomes more acidotic = more abnormalities in venous circulation
lead to intrauterine death
describe umbilical artery doppler *
should be triangles joining up
as get more resistance get more PI, becomes -ve, and reverse flow in umbilical artery
get hypoxia to acidosis
describe the effects of hypoxia *
causes aortic body chemoreceptor stimulation = redistribution of CO = increased flow to brain, heart and adrenals, decreased to lungs kidney and gut
hypoxia causes CNS dysfunction = poor tone, altered breathing, altered movement patterns, chnages in heart rate patterns
middle cerebral artery doppler in hypoxia *
less resistance
want to push the blood to the brain
summarise the fetal circulation *
25% flow from umbilical vein goes to ductus venosis, intrahepatic
fetal perfusion of the renal system = amniotic fluid production
right ventricle is dominant - blood shunted through the foramen ovale
describe ductus venosus doppler *
can see get more severe from hypoxia to acidosis
if see abnormal venous doppler need to deliver in 24-48 hours
describe fetal movement countings *
a reduction in fetal movements may precede fetal death by a day or more
the Cardiff kick chart is the most commonly used
mothers record time taken each day to feel 10 fetal movements
those that report reduction/no need cardiotocography and/or US
bad - cardiotocography line is flat, as it gets worse there are decellerations
how do you manage FGR pregnancies *
problems in the index pregnancy - manage according to serum biochem, fetal doppler, BPP and CTG
screen at risk pregnancies - 24/40 Ut A screening - monitor more regularly (every 2wks and sometimes weekly for dopplers)
aim to deliver when >28weeks and or >500g - c section for comprimised fetuses - timing means balance risk in utero and of preterm birth (decreases as age increases), corticosteroids given for delivery <36wks - might have to deliver because of abnormal CTGs/dopplers/US.maternal comprimise eg uncontrolled high BP
what does mode of delivery depend on *
gestation - cervix might not be ready
condition of the pregnancy
state of the cervix
presentation of the fetus
oligohydramnios
labour may be poorly tolerated due to cord compression and striong contractions - give C section instead
describe early IUGR *
low incidence - 1%
highly correlated to pre-eclampsia
difficult to manage - balancing risk of severe prematurity amd morbidity with risk of IUD
describe late IUGR *
more common 5-7%
rarely correlated to pre-eclampsia
difficult to differentiate from SGA and placenta failure
easy to manage - deliver baby - 30wk survival is about 100%
when are the causes of FGR more prominant *
2nd and 3rd trimester
in 1st all key structures are developing not growing so 50g at end
most of growing happens in 2nd and 3rd
does FGR only occur with pre-eclampsia *
no
can occur without maternal systems, and be because of the placenta or usually defect in fetus
