Abnormal fetal growth Flashcards
Describe the stages of placental development
- Pre-implantation: blastocyst implants, outer trophoblast will become placenta + inner cell mass will be fetus + membranes
- Implantation: trophoblast cells invade endometrium, SCTB erodes maternal tissues + makes hCG
- Post-implantation: SCTB allow blood from spiral arteries to enter forming early U-P circ, CTB forms chorionic villi with embryonic vessels
- Establishment of circulation: remodelling of maternal spiral arteries to make it low resistance + high flow
Describe the umbilical cord
- 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
What causes blood flow between mother + fetus?
- 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
Describe the functions of the placenta
- Gas exchange via simple diffusion
- Fetal nutrition + removal of waste products
- IgG crosses placenta
- Endocrine: produces hCG, human placental lactogen, progesterone, oestrogen
Describe the growth pattern of the fetus
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
CVS system development
Starts as a tube, definitive circulation by 11w, has shunts, CO completely dependent on HR
Respiratory development
- Movements start as early as 12w
- Hypercapnia + raised glucose stimulate, hypoxia + smoking reduce
- Surfactant at functional levels by 32w
Gut development
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
Kidney development
Complete by 36w, GFR increases near end, fetal urine main contributor to AF
Amniotic fluid
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
Why is lying supine in late pregnancy not advisable?
Gravid uterus compresses the IVC - more risk of compromising uterine flow
What factors influence fetal birth weight?
- Gestational age, race, parental height, maternal weight, pariety
- Efficiency of placenta
- Uteroplacental blood flow
What is included in small for gestational age?
- Constitutionally small: below 10th centile, slightly higher risk of comps but not pathological
- IUGR: pathological restriction as the genetic growth potential isn’t reached
What are the types of IUGR?
- Asymmetrical: AC reduced but HC normal, more common, usually later cos of placental insufficiency
- Symmetrical: both AC+HC reduced, more concerning, earlier insult usually
Causes of IUGR
- 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
Complications of IUGR
- Short term: perinatal asphyxiation, meconium aspiration, pulmonary haemorrhage, hypothermia/glycaemia/calcaemia, polycythaemia, jaundice, immunodeficiency, NEC
- Long term: poor growth + development, LD, cerebral palsy
What is large for gestational age?
- Constitutional: HC+AC following the top of the growth chart
- Pathological: macrosomia (HC normal, AC much accelerated) usually due to DM
Define oligohydramnios
Amniotic fluid index <5th centile for gestation
Causes of oligohydramnios
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
What are the risks of oligohydramnios?
- Fetus can’t move properly -muscle contractures
* In PPROM leads to pulmonary hypoplasia so RDS
Define polyhydramnios
AFI >95th centile for the gestation
Causes of polyhydramnios
- 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
CF + comps of polyhydramnios
- 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
Management of polyhydramnios
- 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
