Reproduction 4 - Fetal Growth Flashcards

1
Q

How can size of the fetus be determined?

A
  • Perhaps the simplest to understand are attempts to determine the size of the infant by palpation of the maternal abdomen.
  • This is the basis of determination of the Symphysis Fundal Height (SPH)
  • Distance between the pubic symphysis and the top of the uterus
  • After 20 weeks should be same in cm as the number of weeks
  • At 20 weeks at symphesis puis, 20 weeks at umbilicus
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2
Q

What may cause lower values in symphysis fundal height?

A
  • Wrong last menstrual period date
  • The baby in a transverse lie
  • Complications (including oligohydramnios (low levels of amniotic fluid) or a baby that is small for gestational age (SGA))
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3
Q

What may cause higher values in symphysis fundal height?

A
  • Wrong last menstrual period date
  • Multiple pregnancy
  • Maternal obesity
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4
Q

List complications of large symphysis fundal height

A
  • Molar pregnancy
  • Fibroids
  • Polyhydramnios
  • A baby that is large for gestational age
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5
Q

List pros and cons of symphysis fundal height

A
  • May identify gross changes in size, and hence gross complications in the pregnancy (simple and inexpensive)
  • Is generally of limited use, thanks to the many confounders, such as considerable inter-operator variability, BMI, fetal lie, amniotic fluid and fibroids
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6
Q

List components responsible for the extent of fetal growth

A
  • Genetic potential: this is derived from both parents, as taller parents have larger babies. This will be mediated by factors under genetic control, including mediators such as the insulin-like growth factors.
  • Substrate supply: sufficient nutrients are essential to achieve genetic potential. This is primarily based on the placenta which is dependent upon both uterine and placental vascularity.
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7
Q

How is fetal growth assessed on ultrasound?

A
  • Crown rump length (CRL)
  • Biparietal diameter (BPD)
  • Head Circumference (HC) - used if after 14 weeks or large value for CRL)
  • Abdominal Circumference (AC)
  • Femur Length (FL).
  • Combined to give the Estimated Fetal Weight (EFW).
  • Changes in time plotted to visualise the growth over time. Expected to follow a centile (allows compensation for infants of different sizes)
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8
Q

Why are customised fetal growth charts used?

A
  • They are based on fetal weight curves for normal pregnancies.
  • The are adjusted to reflect maternal constitutional variation e.g. maternal height, weight, ethnicity, parity.
  • They are optimised by presenting a standard free from pathological factors such as diabetes and smoking.
  • Based on normal pregnancies
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9
Q

What is the average velocity an infant gains weight?

A

14-15 wks: 5g /day

20 wks: 10 g/day

32-34 wks: 30-35g/day

> 34 wks: growth rate decreases

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10
Q

List the phases in normal fetal growth

A
  • Cellular hyperplasia (rapid cell division and hyperplasia): 4-20 weeks
  • Hyperplasia and hypertrophy (increased cell size, cell division declines): 20-28 weeks
  • Hypertrophy dominates: 28-40 weeks (rapid increase in cell size, and increase in muscle, fat and connective tissue)
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11
Q

List confounding factors for reliability of the last menstrual period

A
  • Irregular length of periods
  • Abnormal endometrial bleeding
  • The use of oral contraceptives; breastfeeding.
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12
Q

Why is dating of birth important?

A
  • May lead to a pregnancy being inappropriately identified as large or small for gestational age.
  • Clinical decisions about delivery timings and methods (induction or Caesarean section) may not be correct, eg. glucocorticoids are given prior to preterm delivery to enhance lung surfactant production and subsequent lung function.
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13
Q

What is best practice for dating pregnancy?

A
  • Ultrasound, determining the Crown-Rump length (CRL) of the fetus, measuring from the top to bottom.
  • Preferably towards the end of the first trimester
  • Used in all pregnancies except IVF
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14
Q

List maternal factors influencing fetal growth

A
  • Poverty (more likely to have children at a younger age, less aware of risks of factors affecting growth rates, malnutrition)
  • Mothers age
  • Drug use
  • Alcohol
  • Smoking and nicotine
  • Diseases (placenta cannot filter out all pathogens, hypertension, diabetes and coagulopathy)
  • Mothers diet and physical health (eg. lack of iron and anaemia, lack of calcium and poor bone formation, lack of protein and mental retardation)
  • Mothers prenatal depression (slower fetal growth rate)
  • Environmental toxins (eg. lead, mercury and ethanol)
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15
Q

How does mothers age affect fetal growth?

A
  • Women over 35 are more inclined to have a longer labour period, which could potentially result in death of the mother or fetus.
  • Women under 16 and over 35 have a higher risk of preterm labour (premature baby), and this risk increases for women in poverty, African Americans, and women who smoke.
  • Young mothers are more likely to engage in high risk behaviors
  • Premature babies from young mothers are more likely to have neurological defects that will influence their coping capabilities – irritability, trouble sleeping, constant crying for example.
  • There is increased risk of Down syndrome for infants born to those aged over 40 years.
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16
Q

How does drug use affect fetal growth?

A
  • Maternal drug use occurs when drugs ingested by the pregnant woman are metabolized in the placenta and then transmitted to the fetus.
  • When using drugs (narcotics), there is a greater risk of birth defects, low birth weight, and a higher rate of death in infants or stillbirths.
  • Drug use may lead to extreme irritability, crying, and risk for SIDS once the fetus is born, as well as causing addiction
  • Marijuana will slow fetal growth rate and can result in premature delivery.
  • Heroin will cause interrupted fetal development, stillbirths, and can lead to numerous birth defects. (SIDS, miscarriage, abnormal neurological functions)
  • Cocaine use results in a smaller brain and learning disabilities for the fetus. Risk of being stillborn or premature. Cocaine use also results in low birthweight, damage to the central nervous system, and motor dysfunction.
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17
Q

How does alcohol affect the foetus?

A
  • Disruptions of the fetus’s brain development, interferes with the fetus’s cell development and organization, and affects the maturation of the central nervous system.
  • Alcohol use can lead to heart and other major organ defects, such as small brain, which will affect the fetus’s learning behaviors.
  • Alcohol use during pregnancy can cause behavioral problems in a child, mental problems or retardation and facial abnormalities – meaning smaller eyes, thin upper lip, and little groove between the nose and lips. Use can also increase the risk of miscarriages and stillbirths, or low birth weight.
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18
Q

What is fetal alcohol syndrome?

A
  • Fetal alcohol syndrome (FAS) is a developmental disorder that is a consequence of too much alcohol intake by the mother during pregnancy.
  • Children with FAS have a variety of distinctive facial features, brain abnormalities, and cognitive deficits.
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19
Q

How does smoking and nicotine affect the fetus?

A
  • When a mother smokes during pregnancy the fetus is exposed to nicotine, tar, and carbon monoxide.
  • Nicotine results in less blood flow to the fetus because it constricts the blood vessels. (also increases risk of miscarriage)
  • Carbon monoxide reduces the oxygen flow to the fetus.
  • The reduction of blood and oxygen flow results in stillbirth, low birth weight, and ectopic pregnancy. There is an increase of risk of sudden death syndrome (SIDS) in infants.
  • There has been a link from smoking during pregnancy that led to asthma in childhood.
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20
Q

List the feto-placental factors influencing fetal growth

A
  • Gender (males bigger than females)
  • Hormones
  • Genotype
  • Previous pregnancy
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21
Q

How do hormones affect fetal growth?

A
  • Insulin increases mitotic drive and nutrient availability
  • Cortisol affects tissue differentiation and maturation (alteration of gene transcription, induces switch from IGFII to IGFI)
  • Thyroxine affects tissue accredition and differentiation
  • IGFs are mitogenic, stimulating fetal metabolism. IGFII regulates early embryonic development
  • Glucocorticoid affects tissue differentiation and prenatal development of organs
  • EGFs, TGFs, FGFs, interleukins 1 and embryoinic cholinesterases are all important
  • Somatotrophin has a small effect
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22
Q

Define small for gestational age

A

Infant birth weight below 10th centile (also uses fifth or third centile)

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23
Q

Define intrauterine growth restriction

A

Failure of the infant to achieve predetermined potential (IUFR)

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24
Q

Define low birthweight

A

Less than 2.5kg at delivery (can be normal or with presence of fetal growth restriction, where c-section is needed)

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25
Q

Define very low birth weight

A

Less than 1.5kg at delivery

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26
Q

Define extremely low birth weight

A

Less than 1kg at delivery

27
Q

How are infants with IUGR identified?

A
  • Abdominal circumference less than 10th or 3rd centile

- Abnormal fetal doppler (abnormal umbilical artery)

28
Q

List short term risks of babies with IUGR?

A
  • Most common factor in stillborn babies
  • Respiratory distress
  • Intraventricular haemorrhage
  • Sepsis
  • Hypoglycaemia
  • Necrotisin enterocolitis
  • Jaundice
  • Electrolyte imbalance
29
Q

List causes of IUGR

A
  • 2nd/3rd trimester
  • Maternal medical factors
  • Maternal behavioural factors
  • Fetal factors
  • Placental factors
30
Q

Define pre-eclampsia

A
  • Gestational hypertension of at least 140/90 mmHg on two separate occasions ≥4 hours apart
  • Significant proteinurea of at least 300mg in a 24 hour collection arising after the 20th week of gestation in a previously normotensive woman and resolving completely by the 6th week
  • Multisystem disease
31
Q

How are IUGR and pre-ecalmptic pregnancies managed?

A
  • Timing delivery by balancing risks to fetus if it remains in utero, and hazards of prematurity
  • Corticosteroids administered less than 36 weeks to improve neonatal wellbeing and development of the lungs
  • Pre-eclampsia caused by placenta, so the treatment is delivery
  • Emergency C-section may be needed
32
Q

Where did historical data about fetal growth come from?

A

Miscarriage - showed decrease in fetal growth closer to term, however, miscarriages often occur due to abnormal growth so this is inaccurate

33
Q

Define fetal growth

A

Increase in mass that occurs between the end of embryonic period and birth

34
Q

Why is obstetric ultrasound examination important?

A
  • Assessment of fetal wellness not just size
  • Looking at trends in growth
  • Predicting fetal metabolic compromise
  • Anticipating the need to deliver prematurely (facilitates good obstetric management of cases with abnormal fetal growth)
35
Q

How are the centiles used for SGA chosen?

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 FGR, 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 FGR, but some FGR babies may be missed,
    i. e you get a number of false negatives.
  • Parental factors are not considered
36
Q

List the medium term risks of IUGR

A
  • Continuing respiratory problems
  • Developmental delay
  • Special needs schooling
37
Q

List the long term risks of IUGR

A
  • Important factor in stillborn babies
  • Increased risk of intrauterine death in subsequent pregnancies
  • Fetal programming (adult problems later in life)
38
Q

List causes of SGA

A
  • Dating problem (consistant growth, normal dopplers and fluid)
  • Growth may reduce in 2 weeks
  • Fetal abnormality/ infection (5%)
  • Placental insufficiency (20%)
  • Can be pathologic or non-pathologic (small parents)
39
Q

List maternal medical factors causing IUGR

A
  • Hypertension
  • Connective tissue disease
  • Chronic infection
  • Diabetes
  • Anaemia
  • Uterine abnormalities
  • Pre-eclampsia and maternal malignancies
40
Q

List maternal behavioural factors causing IUGR

A
  • Smoking
  • Low weight
  • Poor nutrition
  • Age
  • Alcohol
  • Drugs
  • High altitude
41
Q

List fetal factors causing IUGR

A
  • Multiple pregnancy
  • Structural abnormality
  • Chromosomal abnormalities
  • Intrauterine infection
  • Inborn errors of metabolism
42
Q

List placental factors causing IUGR

A
  • Impaired trophoblast invasion
  • Partial abruption or infarction
  • Chorioamnionitis
  • Placental cysts and placental praevia
43
Q

How does pre-eclampsia occur?

A
  • Diminished remodelling of the spiral arteries by the cytotrophoblast
  • Therefore, there is decreased blood flow and therefore nutrient supply to the placenta and the fetus
  • Fetus releases factors to stimulate increase in maternal blood pressure to increase nutrients reaching the fetus
  • Damage to the placenta results in damage to the maternal kidneys (causing proteinurea),
44
Q

Which fetuses need growth monitoring?

A
  • Previous maternal hypertension
  • Previous FGR
  • Stillbirth
  • Placental Abruption
  • Abnormal serum biochemistry PAPP-A (pregnancy associated plasma protein) <0.3 MoM
  • Reduced symphysis fundal height
  • Maternal systemic disease e.g. hypertension, renal,
    coagulation
  • Antepartum haemorrhage
45
Q

List risks in maternal histories used to predict fetal growth abnormalities

A
  • Poor Obstetric History
  • Primips (first pregnancy)
  • Obese
  • Afro-Carribean / African
  • Strong Family History
  • Essential hypertension
  • Diabetes / Impaired Glucose Tolerance
  • Systemic vascular disease
  • Renal disease
  • Thrombophilias
46
Q

List concerns in index pregnancy

A
  • Abnormal serum biochemistry
  • Reduced symphysis fundal height
  • Maternal systemic disease e.g. PET
  • Antepartum haemorrhage
  • Multiple pregnancy
47
Q

Describe sequence of events in FGR

A
  • Uterine artery placental blood flow resistance will increase (use of uterine artery doppler)
  • Baby will move less to preserve energy
  • Middle cerebral artery resistance decreases to ensure blood reaches the brain (diversion of blood to major organs)
  • Decreased amniotic fluid as the kidneys are shut down
  • Baby becomes acidotic and there are abnormalities in renal development and therefore there can be intrauterine demise
48
Q

How is FGR monitored?

A
  • Fetal movement countings (reduction may precede fetal death)
  • Fetal doppler
  • Use of cardiotocography (uterine contractions and fetal heart rate)
49
Q

What does the mode of delivery depend upon?

A
  • Gestation of the pregnancy
  • Condition of the pregnancy
  • State of the cervix
  • Presentation of the fetus
  • Oligohydramnios
50
Q

Compare early and late IUGR

A
  • Early low incidence 1%, highly correlated to maternal disease (preeclampsia), and difficult to manage (risks of morbidity)
  • Late IUGR more common 5-7%, rarely correlated to pre-eclampsia, difficult to differentiate from SGA, easy to manage (delivery)
51
Q

Compare small for gestational age and intrauterine growth restriction

A
  • SGA birth weight is lower than the population norms from a single measurement, may be pathological or non-pathological. Babies appear small but not malnurished
  • IUGR is inhibition of normal growth potential, implying pathology. Babies appear malnurished. Change in growth over time.
52
Q

What is fetal doppler?

A

A Doppler fetal monitor is a hand-held ultrasound transducer used to detect the flow of blood, if low it suggests IUGR

53
Q

What is a uterine artery doppler?

A
  • Monitors blood flow through the uterine arteries
  • Allows high resistance or slow flow to be identified (4 fold increased risk in development of pre-eclampsia, 3.5 times higher risk of fetal growth restriction)
  • Increased impedance becomes evident only when at least 60% of the placental vascular bed is obliterated
54
Q

What is the main cause of fetal growth restriction?

A

Lack of nutrients

55
Q

When does the majority of fetal growth occur?

A
  • Third trimester (mainly last 20 weeks)

- Disruption in first trimester where organs develop can result in later growth restriction

56
Q

How has low birthweight changed?

A

Little change in percentage of live births in the UK

57
Q

When is the term fetal growth restriciton used?

A
  • Definite evidence growth has altered

- Can only be assessed by serial observation, as growth is a dynamic process of a change of size over time

58
Q

Describe incidence of pre-eclampsia

A
  • Hypertension in 10% pregnancies

- 1-2% severe form (fetal syndrome)

59
Q

How should uterine artery look?

A

Triangles joining up rather than with gaps inbetween

60
Q

How can middle cerebral artery be monitored in pregnancy?

A
  • Middle cerebral artery blood flow resistance decreases in hypoxia (brain sparing)
  • Therefore, increased blood flow seen in doppler
61
Q

Describe fetal circulation

A
  • Umbilical vein has 25% flow to the ductus venosus, intrahepatic and AC growth
  • Fetal lungs inactive in utero so therefore right ventricle is dominant
  • Fetal perfusion of renal system results in amniotic fluid production
62
Q

How can venous doppler be used in FGR?

A
  • If abnormal baby needs to be delivered within 24-48 hours

- Low venous flow if the baby becomes acidotic

63
Q

List the risk factors for preeclampsia

A
  • Previous history of preeclampsia
  • Multiple gestation (i.e., pregnant with more than one baby)
  • History of chronic high blood pressure, diabetes, kidney disease or organ transplant
  • First pregnancy
  • Obesity, particularly with Body Mass Index (BMI) of 30 or greater.
  • Over 35 or under 20 years of age
  • Family history of preeclampsia (i.e., a mother, sister, grandmother or aunt had the disorder)
  • Polycystic ovarian syndrome
  • Lupus or other autoimmune disorders, including rheumatoid arthritis, sarcoidosis and multiple sclerosis
  • In-vitro fertilization
  • Sickle cell disease
  • African American