Intrauterine Growth Retardation Evaluation (FGR)

Doppler in FGR

FGR is suggested if gestational weeks determined by computer programs repeatedly show delay in the growth parameters from the weeks determined by CRL or correct LMP.

That means the intrinsic growth potential, intrinsic capacity of the fetus to grow is restricted, either due to the factors related to mother, fetus or the connecting link, the uteroplacental circulation.

Causes of FGR

Normal uterine artery flow

Persistent protodiastolic notch in uterine artery upto 25 –26 weeks.

Diagnosis of FGR

• Fundal height below 5th percentile – chronic distress is likely
• Biometric findings – depend on the scan in the first trimester – If only in 2nd trimester, depend on least variable parameters. e.g. cerebellar diameter
• Doppler findings – depend on the first scan at 22 – 24 weeks

Physiology of Umbilical artery circulation

Natural protective mechanism

Organs of preference for oxygenated blood

• Heart
• Brain
• Adrenals

Organs of secondary preference

• Lungs
• Skin
• Skeleton
• Digestive system

Reduced umbilical artery flow Pathophysiology

56% of FGR fetuses – altered umbilical artery FVW, but only 52% had altered heamodynamic pattern, because as long as the two primary compensatory mechanisms are sufficient, no change occurs. Increase in umbilical artery resistance is therefore the first sign of hypoxemia induced by altered villous microcirculation but when the cause is not the uteroplacental circulation but it is the maternal hypoxia, the umbilical artery flows may remain normal and still the MCA and CCA flows will be altered.

Centralization of blood flow ‑ Pathophysiology

• Reduced villous circulation upto 75%
• Rise in umbilical artery resistance
• Decreased PO2 in umbilical vein 16 – 17 mm of Hg, with increasing umb. Artery resistance, pH 7.2
• Fall in CCA and MCA resistance

Advanced phase

• 80% reduced villous circulation
• Fetus is already suffering from a degree of hypoxemia and acidosis.
• Hypoxemia in 70-80% of fetuses and acidosis in 40-60% of fetuses
• Loss of fetal reactivity
• Mortality rate is 1 in 4

1. FGR with normal heamodynamic profile

• No immediate decision
• Doppler and biophysical profile repeated every 1-2 weeks

2. FGR with heamodynamic redistribution > 34 weeks

DO NOT PROLONG THE PREGNANCY.

FGR with heamodynamic redistribution 32 – 34 weeks

• Decelerative TNS pattern,< 5beats / mt variability
• Late advanced stage of centralization
• Absent end diastolic flow in umbilical artery
• Altered venous flow patterns
• Termination of pregnancy
• Earlier stage of centralization Doppler and BPP weekly monitoring

FGR with heamodyanamic redistribution — 28-32 weeks

• Decelerative/ silent TNS pattern
• Reverse diastolic flow in umbilical artery
• Altered venous flows
• Terminate pregnancy
• Initial phase of centralization – expectant management with doppler and BPP follow up every 4-5 days

FGR with heamodyanamic redistribution < 28 weeks

Late advanced stage of centralization – termination
Earlier stage – expectant treatment – continue pregnancy as far as possible, at least upto 30 weeks.

Summary

• Uterine artery notch at 25 – 26 weeks : higher risk of FGR
• Rising umbilical artery resistance after 28 weeks – an alerting signal
• Falling MCA resistance – alarming signal
• Reverse flows in umbilical arteries, normalizing of MCA flow and altered venous signals – a firebrigading signal.