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Fetal growth restriction
outlines
• Introduction
• Etiology Fetal growth restriction
• Classification
• Diagnosis
• Management
• Complication
• delivery timing
• fetal surveillance
Introduction
• IUGR ,FGR, and SGA are terms frequently used interchangeably when
describing the small fetus
• Most often SGA refers to the infant, whereas IUGR to the fetus
• Next to prematurity, FGR is the second leading cause of perinatal
mortality
• PNMR in growth-restricted neonates are 6 to 10 times greater, or 120 per
1000 for all cases of FGR and 80 per 1000 after exclusion of anomalous
infants
• As many as 53% of preterm stillbirths and 26% of term stillbirths have FGR
• In survivors, the incidence of intrapartum asphyxia may be as high as 50%.
Definitions
• FGR is suspected when the Sono graphical EFW is below the
tenth percentile (<2SD) for gestational age
• Failure to achieve intrauterine growth potential
• Abdominal circumference <10th percentile
• Flattening of growth curve as judged by clinician
REGULATION OF FETAL GROWTH
 Fetal growth is regulated at multiple levels and requires successful
development of the placental interface between maternal and fetal
compartments.
 Fetal growth is divided into three phases.
 Initial phase =hyperplasia occurs in the first 16 weeks and is cx rapid rise in
cell number.
 Second phase -up to 32 weeks’ gestation, includes both cellular
hyperplasia and hypertrophy.
 Third phase -32 weeks onward , cellular hypertrophy,
 most fetal fat and glycogen accumulate.
 fetal-growth rate 5 g/d at 15 weeks’ gestation,15 g/d at 24 weeks’, and 30
g/d at 34 weeks
Determinants of optimal Fetal growth
• Distance b/n maternal microvillous and fetal basal layers in the placenta
• Rate of oxygen delivery to the uterus and placental blood flow
• a magnitude of maternal nutrient
classification
 Based on absolute birthweight(old)
 low birthweight (LBW; <2500 g),
very low birthweight (VLBW; <1500 g),
extremely low birthweight (ELBW; <1000 g), or
 macrosomia (>4000 g)
 Based birthweight percentile (current)
very small for gestational age (VSGA; <3rd percentile),
small for gestational age (SGA; <10th percentile),
average for gestational age (AGA; 10th to 90th percentile), or
large for gestational age (LGA; >90th percentile).
Draw back
normal birthweight percentile, but abnormal body proportion as a result of differential
growth delay may be missed
Can’t d/t between the const small neonate and growth restricted
 Based on body proportion
Fetal causes
Teratogenic exposure
Fetal infection ≤10%
 Genetic disorders
 Structural abnormalities
Chromosomal abnormalities may be
detected
o 17% of FGR % ,,,,,, some says
less than 1o%
o 66% of u/s confirmed fetal
malformation
o 53 % of trisomy 13 and 64%
trisomy 18
Placental causes
Primary placental disease
Placental abruption and infarction
Placenta previa
Placental mosaicism
Maternal causes
Hypertensive disease
Pregestational diabetes
 Cyanotic cardiac disease
 Autoimmune disease
Restrictive pulmonary ds
Tobacco/substance abuse
High altitude (>10,000 feet)
Malabsorptive ds/malnutrition
 Multiple gestation
Thrombophilia
Drugs eg phenytoin
MANIFESTATIONS OF FETAL GROWTH RESTRICTION
Maternal Impacts
o Due to poor placentation ,
 suboptimal maternal volume expansion,
 increased vascular reactivity, and
 “flat” curve on the glucose tolerance test
Lack of spiral and radial A physiologic transformation into low-resistance vessels
(expected at 22-24wks)
Fetal Impacts
Metabolic manifestations
Initially after oxygen and nutrient deficit ,fetal supply is compromised first,
whereas placental nutrition is preferentially maintained. Both affected later on
If uterine oxygen delivery falls below a critical value (0.6 mmol/kg/ min ),
Fetal hypoxemia or hypoxia
Hypoglycemia
Fetal endocrine manifestations
Low insulin and ILGF –I &II
Low fat stores
Significant elevations of CTRH, ACTH, and cortisol and
Decline in active vitamin D and osteocalcin
Hypothyroidism
Elevations in serum glucagon, adrenaline, and noradrenaline …RF for
adulthood DM
Fetal hematologic response
Polycythemia
 Inc Oxygen carrying and the buffering capacity
elevated NRBC
fetal anemia and thrombocytopenia due to placental consumption
Fetal immune manifestation
the cellular and humoral dysfunction (WBC,IG,B-cells,t-lymphocyte…)
 Fetal cardiovascular responses
Early -adaptive in nature and result in preferential nutrient to essential
organs
dec umbilical venous flow volume ---earliest feature
Elevation of pulm.V bed and subdiaphragmatic circulation of BFR
myocardium and brachiocephalic circulation has been termed
redistribution,
Late -impairment of cardiac function due to worsened SVR
 loss of diastolic forward flow in the umbilical venous circulation
….hallmark
• Finally, myocardial dysfn and cardiac dilatation holosystolic tricuspid
insufficiency and spontaneous FHR decelerations, followed by fetal demise
• Delivery should be below 34wk
 fetal organ Autoregulatory for blood flow
myocardium, adrenal glands, spleen, liver, celiac axis, mesenteric
vessels, and kidney
Fetal behavioral responses
Abn body movements and fetal breathing
BPP abnormality at 28-32wks
DIAGNOSTIC TOOLS IN FGR
 After confirming small fetal size, stratification into three patient
groups is of particular importance.
Constitutionally small=not require antenatal surveillance and
intervention
Fetus with chromosomal or congenital anomaly =need family
counselling
Fetus with placental abnormality =benefit from fetal
surveillance and subsequent intervention
Fetal Biometry
• Accurate FGR measurement need knowledge of GA
I ) fetal head (BPD, HC and TCD)
asymmetric FGR are not diagnosed late
HC is not affected by external factors unlike BPD
TCD relatively spared from the effects of mild to moderate uteroplacental
dysfunction
ii) Abdominal circumference
The AC is the single best measurement for the detection of FGR
higher sensitivity (98% vs. 85%) but lower positive predictive value (PPV) than
the SEFW (36% vs. 51%)
Its sensitivity is further enhanced by serial measurements at least 14 days apart
iii) HC/AC ratio
used for asymmetric FGR
Normally HC/AC ratio > 1 before 32 wks, 1 at 32-34wks , <1 after 34 wks
 the ratio remains high in asymmetric and normal for symmetric
Can detect 70% to 85% of FGR
 sensitivity and PPV is less than AC and SEFW
iv) FL/AC ratio
Used w/n difficult measurement in HC( head position-AP, Breech
,oligohydramnios)
The FL/AC ratio is 22 at GA from 21 weeks to term;
An FL/AC ratio greater than 23.5 suggests FGR.
v) Sonographic estimated fetal weight (SEFW)
The accuracy of most formulae (±2 standard deviations [SDs]) is ±
10%,
has a lower sensitivity but higher PPV than the AC
The most important calculated ultrasound variable
Parameters
Fetal Anatomic Survey
Amniotic Fluid Assessment
-SDP and AFI
 Doppler Velocimetry
1. Arterial Doppler waveforms
• Increase in vascular resistance leads
 S/d ratio, PI ,RI or
absent EDV and REDV
• UA, MCA
2. Venous Doppler parameters
DV,IVC and umbilical
Vi) Invasive Testing
cordocentesis
amniotic fluid R/o TORCH infection and/or karyotyping or
microarray analysis for chromosomal ds
SCREENING AND PREVENTION OF FGR
 Maternal History
 Clinical Examination
 Maternal Serum Analytes
 Maternal Doppler Velocimetry
 Integrated Approach to Screening
Preventive Strategies
 initiation of low dose ASA at 12-16wks GA decrease PE or FGR by 50-
60%
Indications
poor obstetric history,
unexplained elevations in second-trimester MSAFP,
 flat oral glucose tolerance curves, and
abnormal second-trimester uterine artery Doppler velocimetry
MANAGEMENT IN CLINICAL PRACTICE
Conservative managements
Avoid stress, smoking, and alcohol and drug use
Bed rest in the LLP.
Dietary supplementation
Maternal hyperoxygenation
Maternal volume expansion –for low volume status
corticosteroids for lung maturity
Fetal surveillance
ASSESSMENT OF FETAL WELL-BEING
Maternal Monitoring of Fetal Activity
Fetal Heart Rate Analysis … NST,CST
Amniotic Fluid Volume
Biophysical Parameters
Doppler Ultrasound
Invasive Fetal Testing
Timing of delivery
• Depends on :
• the underlying etiology of FGR (if known)
• Estimated GA
• Others like antenatal fetal surveillance
• If delivery is anticipated within 7 days, then administration of
antenatal corticosteroids for fetal lung maturation is indicated in
fetuses diagnosed with growth restriction prior to < 33 6/7 weeks.
• If delivery prior to 32 0/7 is anticipated, then consider
neuroprotection with magnesium sulfate.
• Growth restricted fetuses with abnormal Doppler velocimetry at less
than 32 weeks should be discussed with Maternal Fetal Medicine.
Integrated Fetal Testing and Management Protocol

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IUGR.pptx

  • 2. outlines • Introduction • Etiology Fetal growth restriction • Classification • Diagnosis • Management • Complication • delivery timing • fetal surveillance
  • 3. Introduction • IUGR ,FGR, and SGA are terms frequently used interchangeably when describing the small fetus • Most often SGA refers to the infant, whereas IUGR to the fetus • Next to prematurity, FGR is the second leading cause of perinatal mortality • PNMR in growth-restricted neonates are 6 to 10 times greater, or 120 per 1000 for all cases of FGR and 80 per 1000 after exclusion of anomalous infants • As many as 53% of preterm stillbirths and 26% of term stillbirths have FGR • In survivors, the incidence of intrapartum asphyxia may be as high as 50%.
  • 4. Definitions • FGR is suspected when the Sono graphical EFW is below the tenth percentile (<2SD) for gestational age • Failure to achieve intrauterine growth potential • Abdominal circumference <10th percentile • Flattening of growth curve as judged by clinician
  • 5. REGULATION OF FETAL GROWTH  Fetal growth is regulated at multiple levels and requires successful development of the placental interface between maternal and fetal compartments.  Fetal growth is divided into three phases.  Initial phase =hyperplasia occurs in the first 16 weeks and is cx rapid rise in cell number.  Second phase -up to 32 weeks’ gestation, includes both cellular hyperplasia and hypertrophy.  Third phase -32 weeks onward , cellular hypertrophy,  most fetal fat and glycogen accumulate.  fetal-growth rate 5 g/d at 15 weeks’ gestation,15 g/d at 24 weeks’, and 30 g/d at 34 weeks
  • 6.
  • 7. Determinants of optimal Fetal growth • Distance b/n maternal microvillous and fetal basal layers in the placenta • Rate of oxygen delivery to the uterus and placental blood flow • a magnitude of maternal nutrient
  • 8. classification  Based on absolute birthweight(old)  low birthweight (LBW; <2500 g), very low birthweight (VLBW; <1500 g), extremely low birthweight (ELBW; <1000 g), or  macrosomia (>4000 g)  Based birthweight percentile (current) very small for gestational age (VSGA; <3rd percentile), small for gestational age (SGA; <10th percentile), average for gestational age (AGA; 10th to 90th percentile), or large for gestational age (LGA; >90th percentile). Draw back normal birthweight percentile, but abnormal body proportion as a result of differential growth delay may be missed Can’t d/t between the const small neonate and growth restricted
  • 9.  Based on body proportion
  • 10. Fetal causes Teratogenic exposure Fetal infection ≤10%  Genetic disorders  Structural abnormalities Chromosomal abnormalities may be detected o 17% of FGR % ,,,,,, some says less than 1o% o 66% of u/s confirmed fetal malformation o 53 % of trisomy 13 and 64% trisomy 18 Placental causes Primary placental disease Placental abruption and infarction Placenta previa Placental mosaicism
  • 11. Maternal causes Hypertensive disease Pregestational diabetes  Cyanotic cardiac disease  Autoimmune disease Restrictive pulmonary ds Tobacco/substance abuse High altitude (>10,000 feet) Malabsorptive ds/malnutrition  Multiple gestation Thrombophilia Drugs eg phenytoin
  • 12. MANIFESTATIONS OF FETAL GROWTH RESTRICTION Maternal Impacts o Due to poor placentation ,  suboptimal maternal volume expansion,  increased vascular reactivity, and  “flat” curve on the glucose tolerance test Lack of spiral and radial A physiologic transformation into low-resistance vessels (expected at 22-24wks)
  • 13. Fetal Impacts Metabolic manifestations Initially after oxygen and nutrient deficit ,fetal supply is compromised first, whereas placental nutrition is preferentially maintained. Both affected later on If uterine oxygen delivery falls below a critical value (0.6 mmol/kg/ min ), Fetal hypoxemia or hypoxia Hypoglycemia
  • 14. Fetal endocrine manifestations Low insulin and ILGF –I &II Low fat stores Significant elevations of CTRH, ACTH, and cortisol and Decline in active vitamin D and osteocalcin Hypothyroidism Elevations in serum glucagon, adrenaline, and noradrenaline …RF for adulthood DM
  • 15. Fetal hematologic response Polycythemia  Inc Oxygen carrying and the buffering capacity elevated NRBC fetal anemia and thrombocytopenia due to placental consumption Fetal immune manifestation the cellular and humoral dysfunction (WBC,IG,B-cells,t-lymphocyte…)
  • 16.  Fetal cardiovascular responses Early -adaptive in nature and result in preferential nutrient to essential organs dec umbilical venous flow volume ---earliest feature Elevation of pulm.V bed and subdiaphragmatic circulation of BFR myocardium and brachiocephalic circulation has been termed redistribution, Late -impairment of cardiac function due to worsened SVR  loss of diastolic forward flow in the umbilical venous circulation ….hallmark
  • 17. • Finally, myocardial dysfn and cardiac dilatation holosystolic tricuspid insufficiency and spontaneous FHR decelerations, followed by fetal demise • Delivery should be below 34wk  fetal organ Autoregulatory for blood flow myocardium, adrenal glands, spleen, liver, celiac axis, mesenteric vessels, and kidney Fetal behavioral responses Abn body movements and fetal breathing BPP abnormality at 28-32wks
  • 18. DIAGNOSTIC TOOLS IN FGR  After confirming small fetal size, stratification into three patient groups is of particular importance. Constitutionally small=not require antenatal surveillance and intervention Fetus with chromosomal or congenital anomaly =need family counselling Fetus with placental abnormality =benefit from fetal surveillance and subsequent intervention
  • 19. Fetal Biometry • Accurate FGR measurement need knowledge of GA I ) fetal head (BPD, HC and TCD) asymmetric FGR are not diagnosed late HC is not affected by external factors unlike BPD TCD relatively spared from the effects of mild to moderate uteroplacental dysfunction
  • 20. ii) Abdominal circumference The AC is the single best measurement for the detection of FGR higher sensitivity (98% vs. 85%) but lower positive predictive value (PPV) than the SEFW (36% vs. 51%) Its sensitivity is further enhanced by serial measurements at least 14 days apart iii) HC/AC ratio used for asymmetric FGR Normally HC/AC ratio > 1 before 32 wks, 1 at 32-34wks , <1 after 34 wks  the ratio remains high in asymmetric and normal for symmetric Can detect 70% to 85% of FGR  sensitivity and PPV is less than AC and SEFW
  • 21. iv) FL/AC ratio Used w/n difficult measurement in HC( head position-AP, Breech ,oligohydramnios) The FL/AC ratio is 22 at GA from 21 weeks to term; An FL/AC ratio greater than 23.5 suggests FGR.
  • 22. v) Sonographic estimated fetal weight (SEFW) The accuracy of most formulae (±2 standard deviations [SDs]) is ± 10%, has a lower sensitivity but higher PPV than the AC The most important calculated ultrasound variable
  • 23. Parameters Fetal Anatomic Survey Amniotic Fluid Assessment -SDP and AFI  Doppler Velocimetry 1. Arterial Doppler waveforms • Increase in vascular resistance leads  S/d ratio, PI ,RI or absent EDV and REDV • UA, MCA
  • 24. 2. Venous Doppler parameters DV,IVC and umbilical Vi) Invasive Testing cordocentesis amniotic fluid R/o TORCH infection and/or karyotyping or microarray analysis for chromosomal ds
  • 25. SCREENING AND PREVENTION OF FGR  Maternal History  Clinical Examination  Maternal Serum Analytes  Maternal Doppler Velocimetry  Integrated Approach to Screening
  • 26.
  • 27. Preventive Strategies  initiation of low dose ASA at 12-16wks GA decrease PE or FGR by 50- 60% Indications poor obstetric history, unexplained elevations in second-trimester MSAFP,  flat oral glucose tolerance curves, and abnormal second-trimester uterine artery Doppler velocimetry
  • 28. MANAGEMENT IN CLINICAL PRACTICE Conservative managements Avoid stress, smoking, and alcohol and drug use Bed rest in the LLP. Dietary supplementation Maternal hyperoxygenation Maternal volume expansion –for low volume status corticosteroids for lung maturity
  • 29. Fetal surveillance ASSESSMENT OF FETAL WELL-BEING Maternal Monitoring of Fetal Activity Fetal Heart Rate Analysis … NST,CST Amniotic Fluid Volume Biophysical Parameters Doppler Ultrasound Invasive Fetal Testing
  • 30. Timing of delivery • Depends on : • the underlying etiology of FGR (if known) • Estimated GA • Others like antenatal fetal surveillance
  • 31. • If delivery is anticipated within 7 days, then administration of antenatal corticosteroids for fetal lung maturation is indicated in fetuses diagnosed with growth restriction prior to < 33 6/7 weeks. • If delivery prior to 32 0/7 is anticipated, then consider neuroprotection with magnesium sulfate. • Growth restricted fetuses with abnormal Doppler velocimetry at less than 32 weeks should be discussed with Maternal Fetal Medicine.
  • 32. Integrated Fetal Testing and Management Protocol

Editor's Notes

  1. growth is defined as an irreversible constant increase in size, and development is defined as growth in psychomotor capacity Eighty percent of fetal fat gain is accrued after 28 weeks’ gestation, providing essential body stores in preparation for extrauterine life. From 32 weeks onward, fat stores increase from 3.2% of fetal body weight to 16%, which accounts for the significant reduction in body water content.3 Several possibl
  2. the asymmetric growth pattern, somatic growth (e.g., the abdominal circumference [AC] and lower body) shows significant delay, whereas there is relative or absolute sparing of head growth. Two process , First, liver volume is reduced because of lack of deposition and depletion of glycogen stores as the result of limited nutrient supply, which leads to a decrease in AC. Second, elevations in placental blood flow resistance increase right cardiac afterload and promote diversion of the cardiac output toward the left ventricle because of the parallel arrangement of the fetal circulation and the presence of central shunt, This increases blood and nutrient supply to vital structures in the upper part of the body, presumably resulting in relative “head sparing the symmetric growth pattern, body and head growth are similarly affected.
  3. elevated NRBC counts correlate with metabolic and cardiovascular status and are independent markers for poor perinatal outcome fetal anemia and thrombocytopenia (due to placental consumption
  4. adaptive in nature and result in preferential nutrient streaming to essential organs -dec umbilical venous flow volume ---earliest feature -Elevation of blood flow resistance in the pulmonary vascular bed and subdiaphragmatic circulation -shunting of nutrient-rich blood from the DV through the foramen ovale to the left side of the heart increases, and left ventricular output rises in relation to the right cardiac output -myocardium and brachiocephalic circulation has been termed redistribution, which indicates a compensatory mechanism in response to placental insufficiency
  5. An estimated date of confinement (EDC) should be based on the last menstrual period when the sonographic estimate of gestational age is within the predictive error (7 days in the first, 14 days in the second, and 21 days in the third trimester). Once the EDC is set by this method or by a first-trimester ultrasound, it should not be changed because such practice interferes with the ability to diagnose FGR.
  6. The most accurate AC is the smallest directly measured circumference obtained in a perpendicular plane of the upper abdomen at the level of the hepatic vein between fetal respirations. The AC percentile has both the highest sensitivity and negative predictive value for the sonographic diagnosis of FGR whether defined postnatally by birthweight percentile or ponderal index. gestation. In fetuses with asymmetric growth restriction, the HC remains larger than that of the body and results in an elevated HC/AC ratio,31 whereas the ratio remains normal in symmetric FGR, in which both direct measurements are equally affect
  7. The FL/AC ratio is 22 at GA from 21 weeks to term; therefore this ratio can be applied without knowledge of the gestational age.
  8. In unkown GA the FL/AC ratio and a single amniotic fluid pocket is best method of dx IUGR Up to 96% of fetuses with SDP <1cm may be growth restricted IUGR with abundant AFV suggests aneuploidy or fetal infection,
  9. It is worth stressing that the majority of fetuses defined as growth restricted are constitutionally small and require no intervention. Approximately 15% exhibit symmetric growth restriction attributable to an early fetal insult for which there is no effective therapy. Here, an accurate diagnosis is essential. Finally, approximately 15% of small fetuses have growth restriction as a result of placental disease or reduced uteroplacental blood flow Tobacco smoke contains a number of vasoconstrictive substances. Anecdotally, the authors have observed cases of FGR with absent end-diastolic flow in the UA in which diastolic flow returned upon cessation of maternal smokin abdominal wall defects have been raised with administration in the early first trimeste