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RDA - reproduction, development and aging > fetal growth restriction > Flashcards

fetal growth restriction Flashcards

1
Q

define small for gestational age *

A

birth weight <10th centile

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2
Q

define fetal growth restriction *

A

failure of teh fetus to achieve its predetermined growth potential for various reasons

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3
Q

define low birth weight, very low birth weightm extremely low *

A

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…)

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4
Q

what are the signs of early IUGR (intrauterine growth restriction) *

A

abnormal size and umbilical doppler (blood flow)

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5
Q

describe the relationship between low birth weight (LBW), fetal growth restriction, and preterm delivery*

A

most LBW babies are not growth restricted

many FGR babies are delivered prematurely to prevent still birth

they have closely associated pathologies

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6
Q

describe SGA *

A

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

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7
Q

when should you use the term FGR *

A

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

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8
Q

consequences of FGR/IUGR *

A

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
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9
Q

causes of SGA *

A

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

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10
Q

maternal medical factors causing SGA and FGR *

A

•Chronic hypertension

Connective tissue disease

Severe chronic infection

Diabetes mellitus

Anaemia

Uterine abnormalities

Maternal malignancy

Pre-eclampsia

Thrombophilic defects

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11
Q

maternal behavioural factors causing SGA and FGR *

A

Smoking

Low booking weight (<50 kg)

Poor nutrition

Age <16 or >35 years at delivery

Alcohol

Drugs

High altitude

Social deprivation

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12
Q

placental factors causing SGA and FGR *

A

impared trophoblast invasion

Partial abruption or infarction

Chorioamnionitis

placental cysts

Placenta praevi

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13
Q

fetal factors causing SGA and FGR *

A

Multiple pregnancy

Structural abnormality

Chromosomal abnormalities

Intrauterine (congenital) infection

Inborn errors of metabolism

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14
Q

describe the development of the placenta *

A

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

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15
Q

roles of the placenta *

A

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

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16
Q

describe what causes an increase in the pressure in the system in pre-eclampsia*

A

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

17
Q

describe pre-eclampsia *

A

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

18
Q

define pre-eclampsia *

A

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

19
Q

which fetuses need monitoring *

A

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

20
Q

what is the maternal history of someone whose fetus might have FGR *

A

Poor Obstetric History

Primips

Obese

Afro-Carribean / African

Strong Family History

Essential hypertension

Diabetes / Impaired Glucose Tolerance

Systemic vascular disease

Renal disease

Thrombophilias

21
Q

what is the screening for at risk pregnancies *

A

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

22
Q

describe uterine artery doppler screening *

A

arteries narrow = increased resistance = increased BP to support circulation

see notching in poor uterine blood flow

4x increased risk of PET and FGR

23
Q

what are the sequence of events in FGR *

A

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

24
Q

describe umbilical artery doppler *

A

should be triangles joining up

as get more resistance get more PI, becomes -ve, and reverse flow in umbilical artery

get hypoxia to acidosis

25
Q

describe the effects of hypoxia *

A

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

26
Q

middle cerebral artery doppler in hypoxia *

A

less resistance

want to push the blood to the brain

27
Q

summarise the fetal circulation *

A

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

28
Q

describe ductus venosus doppler *

A

can see get more severe from hypoxia to acidosis

if see abnormal venous doppler need to deliver in 24-48 hours

29
Q

describe fetal movement countings *

A

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

30
Q

how do you manage FGR pregnancies *

A

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

31
Q

what does mode of delivery depend on *

A

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

32
Q

describe early IUGR *

A

low incidence - 1%

highly correlated to pre-eclampsia

difficult to manage - balancing risk of severe prematurity amd morbidity with risk of IUD

33
Q

describe late IUGR *

A

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%

34
Q

when are the causes of FGR more prominant *

A

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

35
Q

does FGR only occur with pre-eclampsia *

A

no

can occur without maternal systems, and be because of the placenta or usually defect in fetus

RDA - reproduction, development and aging (10 decks)

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