Abnormal fetal growth

Question 1

Describe the stages of placental development

Answer 1

1. Pre-implantation: blastocyst implants, outer trophoblast will become placenta + inner cell mass will be fetus + membranes
2. Implantation: trophoblast cells invade endometrium, SCTB erodes maternal tissues + makes hCG
3. Post-implantation: SCTB allow blood from spiral arteries to enter forming early U-P circ, CTB forms chorionic villi with embryonic vessels
4. Establishment of circulation: remodelling of maternal spiral arteries to make it low resistance + high flow

Question 2

Describe the umbilical cord

Answer 2

• 2 arteries - carry deoxygenated blood from fetus to placenta
• 1 vein - oxygenated return to fetus
• Wharton’s jelly surrounds
• Outer layer amniotic epithelium
• Helical vessel growth to reduce risk of torsion

Question 3

What causes blood flow between mother + fetus?

Answer 3

• Fetoplacental circulation: fetal heart + aorta + umbilical vessels (susceptible to acute cord compression, oedema, thrombosis)
• Uterine blood flow: uterine arteries + venous return, impairment is more common

Question 4

Describe the functions of the placenta

Answer 4

• Gas exchange via simple diffusion
• Fetal nutrition + removal of waste products
• IgG crosses placenta
• Endocrine: produces hCG, human placental lactogen, progesterone, oestrogen

Question 5

Describe the growth pattern of the fetus

Answer 5

Rate diminishes towards term

• 12w: basically no SC fat, translucent skin, upper limbs at final relative length
• 16w: longer, lower limbs final relative length, can differentiate external genitalia
• 24w: longer, eyes separated, skin opaque but no SC so wrinkled, fine hair over body, lungs begin surfactant production
• 28w: eyes open, scalp hair

Question 6

CVS system development

Answer 6

Starts as a tube, definitive circulation by 11w, has shunts, CO completely dependent on HR

Question 7

Respiratory development

Answer 7

• Movements start as early as 12w
• Hypercapnia + raised glucose stimulate, hypoxia + smoking reduce
• Surfactant at functional levels by 32w

Question 8

Gut development

Answer 8

By 20w starts functioning
Amylase not present until neonatal
Fetus swallows AF + peristaltic gut movement starts mid-pregnancy
Cells + protein digested in AF - fetal faeces - appears in AF with increasing maturity/fetal stress

Question 9

Kidney development

Answer 9

Complete by 36w, GFR increases near end, fetal urine main contributor to AF

Question 10

Amniotic fluid

Answer 10

Amniotic sac develops in inner cell mass of blastocyst - fluid formed through secretion + transudation initially then in 2nd half mostly fetal urine

It increases till 33w, then from 38w it falls. Fetus breathes, swallows, voids, repeats - any issue with these can cause excess/too little

Question 11

Why is lying supine in late pregnancy not advisable?

Answer 11

Gravid uterus compresses the IVC - more risk of compromising uterine flow

Question 12

What factors influence fetal birth weight?

Answer 12

• Gestational age, race, parental height, maternal weight, pariety
• Efficiency of placenta
• Uteroplacental blood flow

Question 13

What is included in small for gestational age?

Answer 13

• Constitutionally small: below 10th centile, slightly higher risk of comps but not pathological
• IUGR: pathological restriction as the genetic growth potential isn’t reached

Question 14

What are the types of IUGR?

Answer 14

• Asymmetrical: AC reduced but HC normal, more common, usually later cos of placental insufficiency
• Symmetrical: both AC+HC reduced, more concerning, earlier insult usually

Question 15

Causes of IUGR

Answer 15

• Maternal: previous SGA, extremes of age, low BMI, smoking, assisted reproduction, heavy work/starvation during pregnancy
• Placental: chronic abruption, TTTS, PET
• Fetal: chromosomal abnormalities, IEM, major structural issues, congenital infection

Question 16

Complications of IUGR

Answer 16

• Short term: perinatal asphyxiation, meconium aspiration, pulmonary haemorrhage, hypothermia/glycaemia/calcaemia, polycythaemia, jaundice, immunodeficiency, NEC
• Long term: poor growth + development, LD, cerebral palsy

Question 17

What is large for gestational age?

Answer 17

• Constitutional: HC+AC following the top of the growth chart
• Pathological: macrosomia (HC normal, AC much accelerated) usually due to DM

Question 18

Define oligohydramnios

Answer 18

Amniotic fluid index <5th centile for gestation

Question 19

Causes of oligohydramnios

Answer 19

Anything that reduces urine production, blocks output or a leak of amniotic fluid. E.g. PPROM (chronic loss of AF), placental insufficiency (reduced output + production as blood sent away from kidneys), renal agenesis, obstructive uropathy, genetic abnormalities, some viral infections

Question 20

What are the risks of oligohydramnios?

Answer 20

• Fetus can’t move properly -muscle contractures

* In PPROM leads to pulmonary hypoplasia so RDS

Question 21

Define polyhydramnios

Answer 21

AFI >95th centile for the gestation

Question 22

Causes of polyhydramnios

Answer 22

• Around half are idiopathic
• Causes may include oesophageal atresia (fetus can’t swallow), CDH, duodenal atresia, anaemia, fetal hydrops, TTTS, higher lung secretions, lithium salts, macrosomia

Question 23

CF + comps of polyhydramnios

Answer 23

• CF: tense distended uterus, US evidence of high liquor volume, fetal size abnormalities,
• Ix: TORCH screen, doppler, OGTT
• Comps: preterm labour, pain/dyspnoea/N+V in mother, malpresentation (more room to move), PPH higher risk (uterus must contract more), higher risk of cord prolapse

Question 24

Management of polyhydramnios

Answer 24

• Usually none, consider amnioreduction if causing severe SOB in mother or indomethacin can be used to increase water retention up to 32w
• In baby examine for causes and pass NG

Question 25

What is the main reason for regular scans in twin pregnancies?

Answer 25

• 16-24w highest risk of TTTS

* >24w growth restriction