small for gestational age, intauterine growth retardation

intra uterine growth retardation

1. SGA/IUGR/Antenatal
Assessment of Fetal Well-being
(Antepartum Fetal Monitoring).
Dr Francis M GidiriDr Francis M Gidiri
MB.ChB, DFSRH, MRCOG, CCT(O&G) UKMB.ChB, DFSRH, MRCOG, CCT(O&G) UK
Senior Lecturer and ConsultantSenior Lecturer and Consultant
Dept of Obstetrics and GynaecologyDept of Obstetrics and Gynaecology
University of Zimbabwe School of MedicineUniversity of Zimbabwe School of Medicine

2. Definitions
SGA or small for dates:
•A fetus that has failed to achieve a specific biometric or estimated
weight threshold by a specific gestational age.
•The commonly used threshold is the 10
th
centile for abdominal
circumference and EFW. Though the 8
th
and 3
rd
centiles are also
used by some.
•SGA fetuses are a heterogeneous group consisting of :
•Fetuses that have failed to reach their growth potential
(IUGR/FGR).
•Fetuses that are constitutionally small.
•About 50-70% of those with birth weight below 10
th
centile are
constitutionally small and have no problems.
•Please NOTE: Fetuses with IUGR may not be SGA.

3. IUGR
•Failure of a fetus to achieve its genetic growth potential.
•NB appropriate terminology: restriction vs. retardation.
•Should be reserved for fetuses in whom there is definite evidence that
growth has faltered.
•Growth is a dynamic process of a change in size over time. Can only
be assessed by serial observations.
•Fetuses with IUGR may not necessarily be SGA and vice versa.
•Genuine IUGR is a result of malnutrition due to malfunctioning
placenta.
•IUGR likely to assoc with reduced AFV, abnormal UAD waveforms
due to placenta insufficiency.

5. What is the appropriate
reference population?
•Local populations charts vs. national charts.
•Some ethnic groups tend to have smaller babies because of genetic
variations (a constant factor), then local charts would be appropriate.
•However if a local population tends to have smaller babies because
they are deprived and have higher incidence of malnutrition, then
using local charts with lower centiles would classify some fetuses and
neonates as AGA when in fact they are at risk of dysfunction.
•Therefore charts must take into account physiological variation such
as maternal height, booking weight, ethnic group, parity and sex of fetus.
This would increase the specificity of the charts for dysfunction.
•Hence the use of customized growth charts.

6. What are we worried
about?
•The vast majority of term SGA infants have no appreciable morbidity or
mortality
•Stillbirths. (15-fold increase) Of 149 apparently unexplained stillbirths,
41% were found to be SGA (Gardosi et al 1998 BJOG)
•Intrapartum hypoxia. CS for FD increased. Low 5-minute APGARs,
severe acidaemia at delivery. Neonatal resuscitation needing intubation.
•Neonatal complications. Morbidity and mortality. E.g. at 38wks
neonatal mortality for SGA babies is 1% vs.0.2% for AGA babies.
Sepsis. RDS, seizures, IVH.
•Impaired neurodevelopment

7. Implications of growth
restriction
1)Stillbirth
2)Mortality.
3)Hypothermia.
4)Hypoglycaemia.
5)FHR abn in labour
6)Increased operative
ddelivery.
1)Pulmonary
haemorrhage
2)Infection.
3)Encephalopathy.
4)Necrotizing
enterocolitis.
5)Problems in later life_later
slides.

8. Neurodevelopment
•SGA babies and preterm babies are more likely to have long-term
neuro-motor dysfunction than AGA babies of same GA.
•Gross motor dysfunction.
•Minor neurological dysfunction
•Rather than CP which is more common in AGA.
•Increase need for special education at age 9. 34% of SGA and very
preterm infants(<32weeks) vs. 46 AGA able to follow mainstream
education.
•Deficits in academic achievement. Less likely to be in top 15%.
•In adult life, less likely to have professional and managerial jobs even
when adjusted for social class. (Strauss RS, JAMA 2000-26 yr follow-up
of the 1970 British birth Cohort)

9. Complications in Adult life
(Morley and Dwyer. Fetal origins of adult disease. Clin Exp Pharmacol Physiol 2001)
•There is increasing evidence emerging now of
increased incidence of problems in later life. These
are:
•Obesity.
•Non-insulin dependent diabetes mellitus.
•Hypertension.
•Cardiovascular disease.

10. Factors Associated with
IUGR/SGA
•Maternal Medical Factors:
•Cyanotic CHD
•Chronic HPT.
•Hyperthyroidism.
•CTD.
•Severe chronic infection.
•Diabetes mellitus.
•Anaemia.
•Uterine abnormalities.
•Pre-eclampsia.
•Thrombophilias. RR of 18 for ACA. Placental
thrombosis is a common finding. Impaired
trophoblastic function.
•Fetal Factors:
•Genetic factors., the gene for glukcokinase, key in
pancreatic B-cell glucose sensing mechanism.
•Multiple pregnancy
•Structural abnormalities. Any of CVS, VNS,
MSS, GIT GU assoc with having a small
fetus.
•Chromosomal abnormalities. Aneuploidy
•Intrauterine infection. Malaria is the major
cause worldwide. Rubella. CMV, Toxo,
syphilis can affect cell division and growth.
•Inborn errors of metabolism
•Maternal Behavioral Factors
•Smoking. Both active and passive. (babies 100-300g smaller).
Number of cigs. Affects uteroplacental and fetoplacental
circulation. Also toxic metabolites
•Low-booking weight.
•Poor maternal nutrition e.g. the Dutch famine and Leningrad
siege. Preconceptual nutrition also important
•Age <16 or >35 years at delivery.
•Alcohol. Depends on amount.
•Drugs.
•High altitude
•Social deprivation.
•Placental factors:
•Impaired trophoblastic invasion. Acute atherosis, thrombosis,
haemorrhage, infarction assoc with reduced uterine blood flow
and reduction in fetal nutrition.
•Placental abruption/infarction.
•Chorioamnionitis.
•Placental cysts.
•Placenta praevia.
•Wrong dates.

11. Early-onset IUGR (<32 weeks)
The principal differential diagnoses are:
•Chromosomal abnormality or some other genetic/syndromal
problem. (normal uterine artery Doppler findings, normal
AFV, presence of structural abnormality). Offer Karyotyping.
•Congenital infection. Fetal IgM not reliable b4 20/40. Fetal IgG
simply reflects maternal antibody levels. Therefore fetal viral
infections often difficult. PCR. The commonest infection assoc
with IUGR is CMV.(maternal hx of flu-like symptoms or fetal USS
features of CMV: microcephaly, cerebral calcification or echogenic
bowel)
•Uteroplacental dysfunction: reduced AFV, abnormal uterine or
UAD waveforms.

12. Clinical features of late-
onset IUGR
Symmetrical:
•Head and trunk size reduced concomitantly.
•In most cases these neonates represent the
lower end of normal range for size.
•Some may be small due to an early onset
insult during period of general organ growth.
•Usually assoc’ with congenital abnormalities.
Intrauterine infections and environmental
factors

13. Late-onset IUGR (>32
weeks)
•Most likely due to uteroplacental insufficiency.
•Often assoc with pre-eclampsia
•Asymmetrical:
•Fetus responds to inadequate nutrition by invoking adjustments that
maximize survival.
•E.g. redistribution of blood to brain, adrenals and less to kidneys
and liver .
•FAC and fat stores are reduced more than the fetal head.
•Assoc with late onset pathology e.g. Pre-eclampsia or idiopathic
IUGR.

14. Screening for IUGR
•Antenatal care: evaluation starts at booking.
•History: identifies high risk and low risk women as test to identify
IUGR are more sensitive in high risk women such as previous IUGR,
PET, medical disorders (HPT, SLE). Tests perform les well when
applied to low risk women due to lack of specificity.
•Abdominal palpation: .Has low sensitivity and PPV. Performs poorly
in identifying SGA fetuses at delivery with detection rates of 30-50%.
•SFH: after 20 weeks 1cm corresponds to 1 week. The margin of error
is however several cms in both directions. This is a better predictor of
fetal size with sensitivities of 64-86% and PPV of 29-79%.

15. Diagnostic Tests
•Biochemical tests: e.g. a single unexplained raised maternal serum a-FP
raises the risk of subsequent IUGR 5-10 fold.
•USS: Use to detect IUGR and for subsequent assessment of fetus. A
single USS in 3
rd
trimester will not be able to differentiate between SGA
and IUGR. FAC encompassing liver, which reflects glycogen stores is a
more reliable parameter. Performs poorly if used for screening the
general population.
•Doppler of the uterine artery at 18-22wks with early notching. RI >95
th

centile. No place yet in practice. Poor sensitivities and PPV (14-47% and
13-38% respectively).
•Umbilical Artery Doppler: detects those babies at risk of hypoxia which
is a late sign in IUGR. Therefore use in screening not established.

16. Prevention of IUGR
•Commonest risk factor for IUGR is smoking. Therefore all
women should be encouraged to stop and/or reduce.
•Even passive smoking is harmful. Partners.
•Women with previous IUGR are at risk of recurrence.
•Aspirin has been studied in this situation.
•Meta-analysis has shown that early ASA reduced the risk of
IUGR. Benefit greatest if given in dose 100-150mg and
before 17 weeks (Leitich et al 1997-BJOG)

17. Initial Assessment once
IUGR suspected.
•Check gestational age using LMP and any early scans.
•Assess fetal size by USS.
•The diagnosis of impaired growth should only be made on
serial scans. Fetal size measurements should be performed
no more frequently than 2 weekly.
•A thorough survey of the fetus for assoc anomalies.
•Quantify LV by AFI likely to be increased in aneuploidy.
•Doppler studies. If normal likelihood of aneuploidy is high.

18. Fetal Monitoring.
•Serial measurements especially AC, AFV, CTG and Doppler ultrasound.
•Umbilical Doppler Studies. (excellent NPV for perinatal mortality and
morbidity)
•AEDF discriminates IUGR fetuses at high risk of perinatal death from
those at low risk. Fetuses with AEDF are hypoxaemic. This may
appear up to 5 weeks before fetal demise. So decision to deliver preterm
not based on EADF only.
•REDF suggests preterminal fetal condition. These fetuses die within 1-
2 days if not delivered.
•RI=S-D/S, PI=S-D/A
•S/D ratio.
•RI has been shown to be most accurate in predicting poor outcome.

19. Fetal Monitoring.
•Fetal Cerebral Flow:
•The fetus is able to redistribute blood to BRAIN and
HEART at the expense of less vital organs in response
to stress such as hypoxia.
•This is demonstrated by increased FLOW VELOCITY
and decrease RESISTNACE INDEX in the MCA.
•Fetal Aortic Flow
•The descending thoracic aorta waveforms of IUGR
fetuses show increased resistance.
•Also the peak systolic velocity is reduced.

20. Fetal Monitoring.
•Fetal Venous Flow
•Cardiac decompensation with alterations in venous flow
represents an end-stage response.
•There is a good correlation between venous Doppler indices
(DUCTUS VENOSUS and IVC ) and hypoxia.
•Flow Velocity waveforms in ductus venosus showing
REVERSAL of flow at time atrial contraction.
•Pulsatile flow in the UMBILICAL VEIN is a sign of severe
fetal compromise.
•Once venous Dopplers are abnormal it may be too late to
change outcome.

21. Amniotic Fluid Volume
•A reduced AFI (the sum deepest vertical pools of all
4 quadrants) is associated with inreased PNMR.
•Fetal urine production is significantly lower in the
SGA fetus than AGA fetus.
•The degree of reduction in urine production
correlates with both the degree of fetal hypoxia and
smalness.
•Oliguria likely a result of of decreased renal
perfusion in favor of essential organs.

22. Biophysical Profile
•Tone, Movement, Breathing, Heart Rate (CTG) and AFV
•RATIONALE: There is an assoc between chronic fetal compromise and
decreased fetal body and breathing movements
•No longer used widely because.
•Time consuming requiring 40 minutes observation for fetal
breathing movements.
• And studies have shown no benefit over simpler tests.
•The most predictive components are the CTG and AFV which are
standard tests anyway.
•Tyrell et al 1990: found that a persistently abnormal BPP score was
always assoc with absence of EDF in a study of 902 BPP and
Doppler assessments in 250 high risk pregnancies.

23. CTG
•A Cochrane review on 1588 patients using CTG for
antepartum monitoring in high-risk patients showed
no significant reduction in perinatal mortality and
morbidity. There was actually an increased PNMR
due to the false reassurance CTG gives.(Pattison et al
2002)
•Therefore not used alone but in conjunction with
Doppler. Deliver when CTG abnormal in AEDF.

24. Sequence of Changes
•Studies have shown that changes in venous
waveforms predate changes in CTG parameters.
Probably by days.
•Variables become abnormal in the IUGR fetus in a
particular order:

26. Summary of Antenatal
Monitoring of the Fetus
•Fetal movement counting.: Cardiff kick chart.
Mothers record time taken to feel 10 movements
each day. Those with reduced or absent movement
require a CTG and /or USS.
•CTG: Antenatal
•BPP: combines CTG, fetal breathing movements,
fetal body movements, fetal tone, AFV.
•Modified BPP, CTG, AFV, UA Dopplers.

27. Timing of Monitoring
•Dopplers and AFV at least weekly.
•If either is abnormal surveillance is increased to at least
twice weekly or more.
•CTG daily or twice daily if abnormal.
•Growth measurements every 2 weeks.

28. What management
decisions need to be made?
•SGA vs. IUGR.
•What fetal monitoring?.
•When to deliver. Depend on gestation and fetal
condition. Balance the risk of prematurity vs.
intrauterine fetal demise.
•How to deliver. The growth restricted fetus may
already be hypoxic and is more likely to become
hypoxic in labour. Therefore CS should be
considered.