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Rep/Dev/Age > Foetal Growth > Flashcards

Foetal Growth Flashcards

1
Q

What is foetal growth?

A

Foetal growth- increase in mass that occurs between end of embryonic period and birth

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2
Q

What contributes to foetal growth extent?

A

Genetic potential – Both parents contribute. Mediated via growth factors (E.G. IGFs)

Substrate supply – Derived from placenta: dependant upon uterine and placental vascularity

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3
Q

What are the phases of foetal growth?

A

Cellular hyperplasia – weeks 4-20
Hyperplasia and hypertrophy – 24-28
Hypertrophy – 28 to term

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4
Q

What is the rate of foetal weight gain during development?

A

14-15 weeks 5g/day
20 weeks 10g/day
32-34 weeks 30-25g/day
>34 weeks growth rate decreases

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5
Q

What are two methods of measuring growth (without ultrasound) in the antenatal clinic?

A

Abdo palpation

Symphysis fundal height

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6
Q

What would be the expect SFH measurement and position of the foetus at different stages in foetal growth?

A 
12 w: Symphysis pubis 
20w at umbilicus  
20-34w: GA +/- 2cm
36-38w: GA +/- 3cm
>38w: GA +/- 4cm
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7
Q

What could causes the SFH to be lower than expected?

A

Wrong dates (Growth sequence will appear normal)
Small for GA
Oligohydramnios
Lying transverse

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8
Q

What could causes the SFH to be higher than expected?

A 
Wrong dates (Growth sequence will appear normal)
Molar pregnancy 
Multiple gestation
Large for GA 
Polyhydramnios 
Maternal obesity 
Fibroids
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9
Q

What are the pros and cons of SFH?

A

Pros
Simple
Inexpensive

Cons
Low detection rate 50 -856%
Great inter-operator variability
Influenced by many factors: BMI, Foetal lie, amniotic fluid, fibroids

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10
Q

What are the methods of dating pregnancy?

A

Dating by LMP – inaccurate: Irregular periods, abnormal bleeding, oral contraceptive, breastfeeding

Date by crown rump length instead (Except for IVF in which case fertilisation is known)
Head circumference after 14 weeks CRL >84mm

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11
Q

What is the importance of pregnancy dating?

A

Prevent false reads of SGA or LGA
Prevent inappropriate inductions
Ensure steroids used in true preterm delivery

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12
Q

What are the four biometric parameters for measuring foetal growth?

A

BPD – biparietal diameter
HC – Head circumference
AC – Abdominal circumference
FL – Femur length

Normative growth curves constructed from ultrasound measurements – expressed in centiles

These clinically used to assess normal or abnormal intrauterine growth – risk of obstetric and neonatal complication

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13
Q

What factors influence foetal growth?

A 
Maternal 
Poverty
Age 
Drug use
Weight 
Disease
Smoking
Alcohol 
Diet
Prenatal depression 
Toxin environment
Foeto-placental
Genotype
Gender (B>G)
Hormones 
Previous pregnancy
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14
Q

What foetal hormones contribute to growth?

A 
Pituitary – GH (Some, partly via hepatic GFs), FSH/LH
Pancreas – Insulin
Adrenals – Androgens 
Gonads – Androgens
Thyroid – Iodothyronines (3rd trimester)
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15
Q

What is a customised growth chart?

A

The customised standard defines the individual foetal growth potential by three underlying principles:

Adjusted to reflect maternal constitutional variation (maternal height, weight, ethnicity, parity)

Optimised by presenting a standard free from pathological factors such as diabetes and smoking

Based on foetal weight curves derived from normal pregnancies

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16
Q

What are some congenital size abnormalities?

A

Growth restriction
Macrosomia
Achondraplasia (Trunk normal, limbs small)
Neonatal hydrocephalus (Only head large - excess fluid)

17
Q

What is the ultrasound scan of foetus used for?

A

Assessment of foetal “wellness” not just size
Looking at trends in growth
Predicting foetal metabolic compromise
Anticipating the need to deliver prematurely
Liaising with Neonatal Services

18
Q

What are small for gestational age foetuses? How does this vary from foetal growth restriction?

A

The definition for small for gestational age (SGA) is an estimated birth weight that is < 10th centile
The foetal growth restricted (FGR) babies: failure of foetus to achieve its pre-determined potential
The WHO defines the small baby as a baby with a birth weight of less than 2.5 kilograms
Using birth weight alone doesn’t take into account the gestational age (Epidemiological studies don’t measure GA)

Most LBW neonates are NOT growth restricted, and many FGR babies are delivered prematurely
There is a 3-10 fold increase in perinatal mortality in FGR babies
There is also short- and long-term morbidity
LBW, FGR and preterm delivery are closely associated pathologies

19
Q

Which centiles are used to diagnose SGA and FGR?

A

The tenth centile is most sensitive (But has false positives) and the third centile is most specific (But some missed postives)

5th centile can be used

20
Q

What is the distinguishing feature of FGR compared to SGA?

A

FGR - Must observe that growth has ALTERED, need serial measurement and to see stop of growth between (e.g stays same size over two weeks)

21
Q

What are the consequences of FGR?

A

Intrauterine growth restriction (IUGR) is the most common factor identified in stillborn babies
Also serious consequences for babies who survive.
Delivery timing can prevent still births.

(There is an increased risk of IUGR and intrauterine death in mother’s subsequent pregnancy)

22
Q

What are the immediate risks of an infant with LBW/FGR after delivery?

A

Respiratory distress: particularly if developed before 34 weeks (minimised by giving steroid injections)

Intraventricular haemorrhage: produces a risk of cerebral palsy later on

Sepsis: due to an immature immune system

Hypoglycaemia: if the liver is less developed, you see metabolic problems

Necrotising enterocolitis: preferential diversion of blood to other places, resulting in ischaemia

Jaundice

Electrolyte imbalance

23
Q

What may LBW/FGR children experience growing up?

A

Respiratory problems

Developmental delays

24
Q

What are the adult life consequences for LBW/FGR children?

A

Foetal programming – ischaemic heart disease, congenital heart disease and diabetes are more
common, due to compensatory pathways (influenced by initiation by poor growth at the beginning of life)

25
Q

What are the causes of SGA?

A

Most small for gestational age babies are normal - but may just be constitutionally small.

20% due to placental insufficiency - Inadequate nutrients provided (Nutrients will be diverted and abnormal foetal dopplers will be observed)

5% due to foetal problem - This could be a chromosomal abnormality

26
Q

How does the placenta contribute to foetal growth?

A

10-12 weeks is the period of placentation

Rapid early growth prepares way for foetal growth
Trophoblast cells use same molecular mechanisms as tumors, but are highly regulated and controlled
The placenta maintains immunological distance between mother and foetus

Special endocrine organ: produces protein-peptides and steroid hormones
It functions as a “transient hypothalamo-pituitary-gonadal axis”
Responsible for exchange of nutrients, gases & waste products between maternal and fetal circulation

27
Q

How may placental function be disordered in a pregnancy?

A

In a non-pregnant woman, the placenta looks different. The spiral arteries in non-pregnant state sit within the endometrium.

In normotensive, normal pregnancy, the spiral arteries open up. There is a wave of trophoblastic invasion. Trophoblasts invade, to get rid of the muscular wall. There is a funnel shapes, much more dilated
vessel, to accommodate the increased amount of blood flow from mother to baby.

In pre-eclamptic toxaemia, the process of trophoblastic invasion failed. The spiral arteries remain narrow. There is a high shearing force just to get through to the blood supply. This causes ischaemic changes and endothelial imbalance

28
Q

What are the side effects of Pre-eclampsia?

A

PET (Pre-eclampsia toxaemia) is associated with LBW/FGR. Defined as pregnant women who have hypertension, oedema and proteinuria.

Maternal compensatory effects (mother has hypertension to compensate for blood supply)

This is extremely common – there is HBP in 10% of all pregnancies (1-2% suffer a severe form).

Arises de novo. It occurs after the 20th week of gestation in a previously normotensive woman and
resolving completely by the 6th postpartum week.

Foetal syndrome (FGR without pre-eclampsia) is relatively rare.

29
Q

What BP and urine levels may be present in pre-eclampsia?

A

BP>140/90mmHg and proteinuria >0.3g/24hour (PCR>30)

Mild: 140-149/90-99mmHg

Moderate: 150-159/100-109mmHg

Severe: ≥160/110mmHg

30
Q

Why might a foetus need close growth monitoring?

A 
Bad Obstetric History
Previous maternal hypertension
Previous FGR
Stillbirth 
Placental Abruption
Concerns in index pregnancy
Abnormal serum biochemistry
Reduced symphysis fundal height
Maternal systemic disease e.g. hypertension, renal, coagulation
Antepartum haemorrhage
31
Q

What can be used to screen high risk pregnancies?

A

PAPP-A < 0.4 MoM (one of the things we can screen for Down’s syndrome with), POHx PET/FGR

Maternal systemic disease e.g. HT, renal, sickle

Uterine artery Doppler 1st/2nd trimester – blood flow through uterine arteries (This allows us to identify high resistance flow- indicates a higher increase in resistance in the maternal circulation)

32
Q

What in a patient history indicates increased risk of FGR?

A 
Poor Obstetric History
Primips (first pregnancy)
Obese
Afro-Caribbean / African
Strong Family History
Essential hypertension
Diabetes / Impaired Glucose Tolerance
Systemic vascular disease
Renal disease
Thrombophilias
33
Q

How can FGR lead to emergency delivery?

A

Normal maternal circulation - high shearing forces at placenta. If placenta fails, higher resistance within the umbilical artery. The baby begins to stop growing,
causing reduction in foetal movements.

Baby tries to compensate - diverts blood to the vital organs. Shuts down supply to the kidneys, resulting in less amniotic fluid. Causes decompensation. Needs immediate delivery to prevent intrauterine death.

34
Q

What changes in bloodflow will be observed in FGR?

A

Doppler ultrasound techniques looks at different arteries. Umbilical arteries give idea of placental blood flow. Increased impedance becomes evident only when at least 60% of the placental vascular bed is obliterated.

As the baby becomes more hypoxic, there is
high resistance to virtually no end diastolic flow. Reversible flow results as the baby becomes more acidotic.

The baby also slows down movements. Eventually, we see heart range changes on the CTG. As the baby becomes more hypoxic, there is lower resistance to blood flow in the brain (e.g. middle cerebral artery).

35
Q

How does the ductus venosus change in hypoxia?

A

The umbilical vein diverts 25% of its flow to the ductus venosus. As the baby becomes more and more hypoxic, it goes from a normal, low resistant pattern to a HIGH resistance pattern

36
Q

How are foetal movements used to assess foetal health?

A

A reduction in foetal movements may precede foetal death by a day or more

Cardiff kick chart is the most commonly used method UK. Mothers record time to feel ten foetal movements daily

Reduction (or absence) in foetal movements, requires cardiotocography and/or an ultrasound assessment of the foetus to ensure foetal wellbeing. Foetal heart rate
monitored using CTG.

37
Q

How is delivery date decided in FGR pregnancies?

A

Timing delivery in these pregnancies depends on balancing the risks to the foetus if it remains in utero
and the hazards from the prematurity, which decrease as the gestation advances

Evidence of foetal compromise on CTGs or abnormal Dopplers/ultrasound finding/maternal compromise

Corticosteroids should be administered (if not already given) at gestations < 36 weeks in order to
improve neonatal wellbeing

(Labour may be poorly tolerated due to cord compression)

38
Q

What are the two different categories of IUGR?

A

Early IUGR:
This has a low incidence (1%)
Highly correlated to maternal disease (pre-eclampsia)
Difficult to manage: balancing risks of severe prematurity and morbidity with risk of in utero death

Late IUGR:
More common (5-7%)
Rarely correlated to pre-eclampsia
Difficult to differentiate from constitutionally SGA
Easy to manage: deliver

Rep/Dev/Age (8 decks)

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