Progress in Obstetrics & Gynecology (Volume 3) Narendra Malhotra, Arun Nagrath, Shikha Seth
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OBSTETRICS

Fetal Growth Restriction and Fetal Compromise: Management Basis and Strategy1

Narendra Malhotra
Jaideep Malhotra
JP Rao
Sakshi Tomar
 
DEFINITION
Fetal growth restriction (FGR) previously defined as intrauterine growth retardation or IUGR, is a pathological decrease in the rate of fetal growth. It means that the fetus is not growing properly; it does not imply hypoxia or acidosis. It is possible to assesfetal growth accurately by B mode, 2D, gray scale ultrasound. Addition of color Doppler gives information about fetal oxygenation, hypoxia and acidosis and 3D/4D ultrasound picks up subtle soft tissue markers for growth restriction. Fetal compromise is defined as a hypoxemic, hypoxic or acidotic fetus; this is a pathophysiological detoriation of many of the FGR fetuses.1
Fetal compromise is diagnosed by Doppler flow velocimetry of uterine, placental and fetal circulation. Doppler picks up compromise earlier than biophysical profile or nonstress testing.2–4
 
ETIOLOGY
Fetal growth restriction is due to:
  1. Fetal causes.
  2. Placental causes.
  3. Maternal causes.
Fetal growth restriction (FGR) is not a disease entity by itself and results as a outcome of impaired nutritional supply to fetus due to the above three causes which may be genetic and nongenetic anomalies, fetal infections, SLE and maternal hypertension.
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PATHOPHYSIOLOGY
Whenever there is a less supply of nutrition and oxygen to the fetus the fetus cardiac dynamics get altered and a redistribution of blood to cerebral vessels and cardiac vessels occur, shutting down the aortic blood flow and splanchnic blood flows this causes less nutrients and oxygen to go to the fetal organs and hence restricts the growth of muscles and bones making the fetus small. Finally the renal blood flow and blood flow to intestines is also affected leading to oligohydramnios and also may lead to necrotizing entrocolitis and/or muconium aspiration. While the brain receives compensatory blood flows and leads to a brain sparing effect in the growth. Finally the cerebral vessels get constricted due to cerebral edema and due to not receiving oxygen and nutrients and this is the end stage FGR which will lead to cardiac failure and fetal death.
 
FETAL GROWTH RATES
Ultrasound estimation of fetal growth parameters and fetal weight estimations are the most important screening methods. Fetal weight for gestational age curves are used to identify growth rates for diagnosis for FGR. If the insult to nutritional supply to fetus is in early pregnancy, i.e. before 20 weeks then all fetal organs show growth restriction proportionately and this is labeled as symmetrical fetal growth restriction (Poor prognosis). The causes for symmetrical growth restriction are:
  1. Fetal anomalies.
  2. Chromosomal (genetic).
  3. Infective fetal pathology.
If the nutrition to fetus is reduced at a later stage in pregnancy, i.e. after 20 weeks due to faulty placentation and uteroplacental insufficiency, then this fetus will show disproportionate growth of fetal abdomen and head and this is labeled as asymmetrical fetal growth restriction. (Proper management can salvage these pregnancies). The causes for utero placental insufficiency are:5
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DIAGNOSIS OF FETAL GROWTH RESTRICTION
Ultrasound measurement of fetal growth parameters and fetal weight estimation is the most common and reliable method of screening for suspected fetal growth restriction. The most common parameters used are BPD, FL, HC, AC. Serial evaluation of fetal growth and additional Sonographic evaluation are necessary to confirm diagnosis of FGR and also identify the etiology. Ultrasound assessment of fetal growth rate at specific intervals will tell us that the growth is normal or it is retarded. If growth rate is normal and fetus is small then there is greater possibility of preterm pregnancy. Fetal growth patterns do not necessarily reflect fetal condition or fetal well being. Fetal biometry will not detect antenatal asphyxia it will detect only a small fetus. To diagnose fetal compromise we need tests to detect fetal oxygenation by studying fetal CNS functions (Flow charts 1.1 to 1.5).6
 
DIAGNOSIS OF FETAL COMPROMISE OR JEOPARDY
The main aim of antenatal care is to identify fetus “at risk”. Fetal compromise can be diagnosed by:
  1. Fetal biometry (Slowing of growth).
  2. Oligohydramnios, AFI of < 5.
  3. Biophysical profile score of Manning or modified biophysical profile by Vintzello's.
  4. Color Doppler studies of maternal, umbilical and fetal vessels.
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Flow chart 1.1: Fetomaternal exchange unit
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Flow chart 1.2: Pathophysiology
Doppler ultrasound is a noninvasive technique to measure the movement of blood (RBCs) in a blood vessel. Out of the available tests for fetal well-being assessment, Doppler ultrasound provides earlier recoginication and more accurate warning of fetal jeopardy (Flow chart 1.5).7
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Flow chart 1.3: Early pregnancy FGR
Test for fetal well-being:
  1. Fetal movement kick count.
  2. Nonstress test.
  3. Contraction stress test or OCT (oxytocin challenge test).
  4. Vibroacoustic stimulation test (VAST).
  5. Manning score (BPP).
  6. Estimation of AFI.
  7. Modified BPP (Vintzelo's).
    6
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    Flow chart 1.4: Mid pregnancy FGR
  8. Ultrasound biometry.
  9. Color Doppler.
  10. 3D and 4D ultrasound.
Indications of fetal well-being studies:
  1. Unexplained previous fetal death.
  2. Decreased fetal movements.
  3. Maternal hypertension.
  4. Pre-eclampsia and PIH.
  5. Maternal diabetes mellitus.
    7
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    Flow chart 1.5: Assessment of maternoplacental fetal unit by color Doppler
  6. Maternal chronic renal disease.
  7. Maternal heart disease.
  8. Rh- or other isoimmunization.
  9. Hemoglobinopathies.
  10. Immunological disorder.
  11. Oligohydramnios.
  12. Polyhydramnios.
  13. FGR (IUGR) clinically.
  14. Multiple gestation.
  15. Post-date pregnancy.
  16. Preterm labor.
  17. PROM (premature rupture of membranes).
  18. History of bleeding in first trimester.
  19. Elderly women.
  20. ART pregnancies.
 
SEQUENTIAL CHANGES IN TESTS FOR FETAL WELL-BEING8,9(FIG. 1.1)
Doppler ultrasound help in study of10 (Flow chart 1.6):
  1. Fetal blood vessels
    • Fetal echocardiography
    • Fetal MCA (Middle cerebral artery)
    • Fetal aorta
      8
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      Fig. 1.1: Sequential changes in tests of fetal well-being in uteroplacental failure (Reproduced with permission)
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      Flow chart 1.6: FGR and IUGR detection
      9
    • Fetal renal artery
    • Fetal venous system
  2. Fetoplacental unit
    • Umbilical artery
  3. Placentomaternal unit
    • Uterine arteries.
It has to be remembered that the fetal aorta carries mixed blood from the fetus to the common iliac to umbilical arteries towards the placenta. Placenta purifies this blood adds nutrition and oxygenation and then this blood goes in umbilical vein to fetal liver. Umbilical vein divides into two portal veins and here 70% of pure blood goes through the ductus venosus into inferior vena cava and into right atrium and through foramen ovale into left atrium and left ventricle and to aorta. Rest 30% pure blood supplies liver tissue for metabolism of nutrients (Fig. 1.2).
The markers for fetal distress hypoxia are:
Chronic distress marker
— Amniotic fluid
Acute distress markers
— Cardiac rate
— Fetal tone
— Fetal movements
— Fetal breathing movements
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Fig. 1.2: Fetal circulation (Reproduced with permission) (For color version, see Plate 1)
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Hypoxia markers are:
Abnormal NST
:
≥ 7.20 pH of umbilical artery
FBM ↓
:
7.20
FM ↓
:
7.10-7.20
Fetal Tone ↓
:
< 7.10
A fetal biophysical profile as suggested by Manning included the monitoring of:
  1. NST (Nonstress test).
  2. FBM (Fetal breathing movements).
  3. FM (Fetal movements).
  4. FT (Fetal tone).
  5. AFI (Amniotic fluid index).
It has been observed that oligohydramnios or ↓AFI indicates an abnormal BPP irrespective of the other four variables, hence to simplify Vintzello et al, suggested a modified BPP with only two parameters.
  1. VAST (Visual acoustic stimulation test).
  2. AFI (Amniotic fluid index).
 
Fetal Oxygenation11
Oxygen crosses from maternal circulation to fetal circulation through a process of facilitated diffusion. Maternal uterine arterial blood enters placenta with a high PO2 and fetal umbilical artery blood enters with a low PO2. Umbilical venous PO2 increases and becomes almost same as uterine venous PO2 (never exceeds) thus umbilical venous PO2 (not higher than mother's) transports enough oxygen to fetal tissues.
  1. High affinity of fetal hemoglobin.
  2. Fetal organ perfusion always exceeds the requirement.
The normal fetal PO2 is 20-25 mm Hg and normal fetal scalp pH is above 7.25. For an adult these might suggest hypoxic values. The fetus becomes hypoxic only when the fetal oxygenation drops below critical levels.
Oxygen uptake by fetus exceeds what is needed and the fetal oxygen delivery can be reduced by 50% before fetal tissue perfusion gets affected. Only then fetus has hypoxia and anaerobic metabolism. Fetus has a “oxygen reserve” (Flow chart 1.7).
 
HYPOXEMIA
When circulating oxygen is reduced and tissue perfusion of oxygen is normal. Fetal PO2 falls to critical level of 19 mm Hg (18-19) fetal pH ranges between 7.25 and 7.20.
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Flow chart 1.7: Oxygenation and fetus
This leads to some compensatory saving mechanisms by increase of left heart cardiac output leading to increased and preferential perfusion of brain and heart these will show as:
  1. Altered cardiac velocities (Fetal echocardiography)
  2. Low resistance cerebral flow (MCA ↓ RI)
  3. High resistance umbilical flow (↑ RI of UA)
Nonstress test changes do not occur at this stage.
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HYPOXIA
When fetal oxygen supply drops to surpass the oxygen reserve. Fetal PO2 drops to 16–17 mm Hg and this leads to tissue hypoxia. The metabolism changes to anaerobic and the scalp pH falls to 7.20 and below.
These changes will show as:
  1. AEDF in umbilical artery
  2. Increased blood flow in middle cerebral
  3. Abnormal NST
  4. May be reduced fetal movements
  5. Amniotic fluid slightly reduced or even normal
  6. Fetal heart variability still maintained
  7. Reduced blood flow in fetal aorta.
 
ASPHYXIA OR ACIDOSIS12
If fetal oxygenation further detoriates there is severe tissue hypoxia. Fetal PO2 falls to 16 or even less and pH 7.10–7.20. Fetal lactic acidosis and academia occurs these changes will show as:
  1. AEDF/REDF in umbilical artery
  2. AEDF in fetal aorta
  3. High resistance in MCA (cerebral decomposition)
  4. Altered ductus venosus and fetal inferior vena cava flows
  5. Marked oligohydramnios (AFI <5)
  6. Abnormal NST (Flat, nonreactive pattern)
  7. Loss of fetal heart variability
  8. No fetal movements
  9. Reduced fetal tone (fetus lying limp).
 
CONCLUSION
Fetal and maternal Doppler examination gives an early and reliable warning of the fetal perfusion status and hypoxemia, Hypoxic and acidosis can be diagnosed by color Doppler examination. Uterine a Doppler is different. It is a screening kept to distinguish women at risk to develop PIH and IUGR. Uterine a study in low risk cases amounts to preventive obstetrics Doppler ultrasound is a noninvasive technique used in obstetrics to improve perinatal outcome in high-risk situations. There are accepted tools in diagnosis and management of FGR fetuses (Flow chart 1.8) and help reducing perinatal mortality. It is important to remember that obstetric management should not be solely based on abnormal Doppler.
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Flow chart 1.8: Management protocols for FGR
All possible clinical, biochemical and Doppler information should be put together along with the “art” of obstetrics to get the best possible outcome.
REFERENCES
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  1. Arduini D, Rizzo G, Romanini C, et al. Fetal blood flow velocity waveforms as predictors of growth retardation. Obstet Gynecol. 1987;70:7–10.
  1. Bercomtz GS, Chitkara U, Rosenberg J, et al. Sonographic estimation of fetal weight and Doppler analysis of umbilical a velocimetry in prediction of intrauterine growth retardation: A prospective study. Am J Obstet Gynecol. 1988;158:1149–53.
  1. O'Shaughnessy RW. Uterine blood flow and fetal growth. In: Fetal growth retardation, FA Van Assche, WB Robertson (eds). Churchill Livingstone,  Edinburgh,  1981.
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  1. Arduni D, Rizzo G. Normal values of pulsatility index from fetal vessels: a cross sectional study on 1556 healthy fetuses. J Perinat Med. 1990, 18: 165–71.
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