Fetal growth Flashcards

1
Q

What does foetal growth depend on? (x2)

A

• GENETIC POTENTIAL: derived from both parents. Genetics control growth factors such as insulin-like growth factors. • SUBSTRATE SUPPLY: essential to achieve genetic potential. Derived from placenta which is dependent upon both uterine and placental vascularity.

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2
Q

What three cellular phases that characterise normal foetal growth?

A
  1. First trimester: Cellular hyperplasia. 2. Second trimester: Hyperplasia and hypertrophy. 3. Third trimester: Hypertrophy alone (key for weight gain).
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3
Q

How does weight change during foetal growth?

A

Velocity of weight gain increases such that by 34 weeks, baby is gaining 30-35g per day. From 34 weeks, this rate slows.

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4
Q

What is Symphysis fundal height (SFH)?

A

Measures distance over abdominal wall from the symphysis to the top of the uterus. It is a way of dating the pregnancy and monitoring foetal growth.

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5
Q

What are the pros and cons of SFH as a measure of foetal growth? (x2 and x3)

A

PROS: simple and inexpensive; CONS: low detection rate, greater inter-operator variability and influenced by several factors such as BMI, foetal lying position, amniotic fluid and fibroids (muscular tumours that grow in the wall of the uterus).

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6
Q

What may the reasons for low SFH be? (x4)

A

Wrong last menstrual period date, the baby in a transverse lie, or complications including oligohydramnios (low levels of amniotic fluid) or a baby that is small for gestational age (SGA).

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7
Q

What may the reasons for high SFH be? (x6)

A

Wrong last menstrual period date, multiple pregnancy, or maternal obesity. Or from molar pregnancy (an abnormal form of pregnancy in which a non-viable fertilized egg implants in the uterus and will fail to come to term. A molar pregnancy is a gestational trophoblastic disease which grows into a mass in the uterus that has swollen chorionic villi), fibroids or a baby that is large for gestational age (LGA).

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8
Q

How were pregnancies conventionally dated? Confounding factors? (x4)

A

Used to use LMP (last menstrual period): however, this can be inaccurate if a woman has irregular periods, abnormal bleeding, is on oral contraceptives or breastfeeding.

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9
Q

How are pregnancies dated now?

A

All pregnancies are now dated by CRL (crown-rump length (length of the embryo/foetus from the crown (head) to the rump (buttocks)). It is determined by ultrasound imaging and used to estimate GESTATIONAL AGE.

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10
Q

How is foetal weight estimated? (x4)

A

Foetal growth i.e. weight, is assessed using four biometrical parameters: BPD (biparietal diameter – diameter across skull), HC (head circumference), AC (abdominal circumference) and FL (femur length). Normal weight curves are constructed from these ultrasound measurements and expressed in centiles. They are used clinically to identify intrauterine growth.

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11
Q

What maternal factors affect foetal growth? (x10)

A

• Poverty – more likely to have children at a younger age. Many of these expecting mothers have little education and are therefore less aware of the risks of smoking, alcohol, and drugs. Women in poverty are more likely to have diseases that are harmful to the foetus too. • Age – women under 16 or over 35. • Drug use. • Weight. • Disease – hypertension, diabetes and coagulopathy. • Smoking and nicotine – nicotine constricts blood vessels and CO reduces O2 flow. • Alcohol – disrupts brain development and increases risk of LBW and miscarriage. • Diet. • Prenatal depression – associated with cortisol levels leading to slower foetal growth rates. • Environmental toxins.

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12
Q

What feto-placental factors affect foetal growth?

A

• Genotype – genetic potential. • Gender (girls more susceptible to undergrowth). • Hormones. • Previous pregnancies.

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13
Q

What are customised growth charts?

A

Growth charts for individual foetus, adjusted to reflect maternal characteristics (height, weight, ethnicity.

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14
Q

What is the definition of Small for gestational age (SGA)?

A

The infant has a birth weight of less than the 10th percentile aka Small for dates. The weight ACCOUNTS FOR GESTATIONAL AGE e.g. an infant of 2,500g at term would be considered SGA, whereas if delivered at 33 weeks this would be an appropriate weight for a normal infant.

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15
Q

What is low birthweight?

A

LBW: less than 2.5kg at delivery.

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16
Q

What is very low birthweight?

A

VLBW: less than 1.5kg at delivery.

17
Q

What is extremely low birthweight?

A

ELBW: less than 1kg at delivery.

18
Q

What is IUGR?

A

Intra-uterine growth restriction: Failure of the infant to achieve its predetermined (genetic) potential. Growth restricted babies are different from babies born early with low birthweight.

19
Q

What is the sensitivity and specificity of centile charts for assessment of IUGR?

A
  • When choosing which centile to use, a balance between sensitivity and specificity is being made – the tenth centile is most sensitive, and the third centile is most specific.
  • The tenth centile will capture all babies with IUGR but will also include those babies that are just small for gestational age, i.e. you get a number of false positives.
  • All babies recorded using the third centile will have IUGR, but some IUGR babies may be missed, i.e. you get a number of false negatives.
20
Q

How is IUGR (growth restriction) accurately assessed?

A

IUGR should only be diagnosed if there is evidence that growth has ALTERED. Growth is a dynamic process of a change of size over time and, therefore, it can only be assessed by serial observation. Serial measurements show that the infant is not growing ALONG A CENTRILE – so, they are growing less than would be expected.

21
Q

What are the short-term (x7), medium-term (x3) and long-term problems associated with IUGF and low birthweight?

A

• SHORT-TERM: respiratory distress, intraventricular haemorrhage, sepsis, hypoglycaemia, necrotising enterocolitis, jaundice and electrolyte imbalance. • MEDIUM-TERM: respiratory problems, developmental delay and special needs schooling. • LONG-TERM: foetal programming (foetal programming is a theory which suggests that the environment surrounding a foetus during its developmental phase plays a role in determining disease risk in later life i.e. IUGR predisposes baby to many diseases in later life such as diabetes).

22
Q

What trimesters are associated with IUGR?

A

Develops in the second and third trimesters of pregnancy. The first trimester concentrates on the development of the embryonic and foetal structures. Almost all weight gain occurs in these latter trimesters.

23
Q

What are the causes of IUGR and the SGA foetus? Four categorisations? (x9, x8, x5, x5)

A

• MATERNAL MEDICAL FACTORS: chronic hypertension, connective tissue disease, severe chronic infection, diabetes mellitus, anaemia, uterine abnormalities, maternal malignancy, pre-eclampsia and thrombophilic defects. • MATERNAL BEHAVIOURAL FACTORS: smoking, look booking weight, poor nutrition, less than 16 years or more than 35 years, alcohol, drugs, high altitude and social deprivation. • FOETAL FACTORS: multiple pregnancy, structural abnormality, chromosomal abnormalities, intrauterine (congenital) infection, inborn errors of metabolism. • PLACENTAL FACTORS: impaired trophoblast invasion, partial abruption or infarction, chorioamnionitis (intra-amniotic infection), placental cysts and placenta praevia (placental attachment position is abnormal e.g. over cervical opening).

24
Q

What is pre-eclampsia? !

A

Aka pre-eclamptic toxaemia (PET): gestational HYPERTENSION of at least 140/90 mmHg, significant PROTEINURIA, arising spontaneously (DE NOVO) after the 20th WEEK of gestation, and resolving completely by the 6th POSTPARTUM WEEK.

25
Q

How is pre-eclampsia linked to IUGR?

A

Pre-eclampsia is mainly caused by diminished remodelling of the spiral arteries by cytotrophoblasts, which causes decreased blood flow and hence decreased nutrient supply to the placenta and foetus – hence, growth of the foetus is restricted = IUGR.

26
Q

How is IUGR and pre-eclampsia managed? (x2)

A

Glucocorticoids (class of corticosteroids) should be administered (if not already given) at gestations <36 weeks in order to improve neonatal wellbeing, notably the development of the lung surfactant. In the case of pre-eclampsia (with or without IUGR), as the placenta is the primary cause, the ultimate ‘treatment’ is delivery. As indicated above, it is the balance between risks that is important in making the decision about the TIMING of delivery.

27
Q

What factors are considered for at-risk-IUGR foetuses? (x2 (x4 and x5)) !

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 such as hypertension, and antepartum haemorrhage (occurring not long before childbirth), multiple pregnancy.

28
Q

What screening identifies at-risk pregnancies? (x3) !

A

• PAPP-A less than 0.3 MoM (pregnancy associated plasma protein A). • Maternal systemic disease. • Uterine artery doppler in the first/second trimester – blood flow through uterine arteries: identify high resistance flow.

29
Q

What does an abnormal uterine artery doppler look like? !

A

High resistance is abnormal and indicated by early diastolic notch and poor diastolic flow.

30
Q

What is the pathophysiology of IUGR (or FGR)? In relation to UtA Doppler?

A
  1. Pi is a measure of perfusion. It is measured as peak systolic flow – peak diastolic flow. Higher levels of Pi indicate poorer perfusion. It is assessed using the UtA doppler.
  2. Uterine artery narrowing leads to high resistance and subsequent high Pi in umbilical artery.
  3. This leads to HYPOXIA. The foetus responds with CNS DYSFUNCTION and AORTIC BODY CHEMORECEPTOR STIMULATION.
  4. CNS DYSFUNCTION alters foetal movement patterns and breathing to conserve energy.
  5. AORTIC BODY CHEMORECEPTOR STIMULATION redistributes cardiac output, increasing flow to the brain, heart and adrenals; diverting blood from the lungs, kidneys and gut.
  6. Decreased renal perfusion leads to reduced production of amniotic fluid and baby becomes acidotic which leads to abnormalities in the venous circuit.
  7. These all lead to FGR/IUGR. NB: The nature of blood flow explains the complications of IUGR. PAY ATTENTION TO PHOTO.
31
Q

What is CTG monitoring?

A

Cardiotocography (CTG) records foetal heartbeat to assess foetal wellbeing.

32
Q

What is the difference between early and late IUGR?

A

• EARLY IUGR: has onset early on in pregnancy, is least common, and highly correlated to preeclampsia. It is difficult to manage – there is difficulty balancing the risks of severe prematurity and morbidity with risk of in utero death. • LATE IUGR: has onset later in pregnancy, is more common, and rarely correlated to preeclampsia. It is difficult to differentiate from SGA and easier to manage.