Key words
fetal growth restriction (FGR) - intrauterine growth restriction (IUGR) - small for
gestational age (SGA) - Doppler sonography - computerised cardiotocography
Introduction
Growth of the healthy fetus usually follows a linear pattern, i.e., with constant
percentile growth, thus exploiting its genetically determined growth potential. A
fetus diagnosed to be small at ultrasound requires a structured diagnostic work-up
in order to achieve an optimal ante- and perinatal management.
Fetal or intrauterine growth restriction (FGR/IUGR) affects approximately 5 – 8% of
all pregnancies and refers to a fetus not exploiting its genetically determined growth
potential. Presently, FGR is classified into early (early-onset < 32 + 0 weeks of
gestation [wks]) and late FGR (late-onset ≥ 32 + 0 wks) [1]. FGR is one of the main causes of perinatal morbidity and mortality, and this is
especially true when fetal growth problems are not recognised as such before delivery
[2]. Moreover, fetal growth restriction apparently predisposes to the development of
chronic disorders in later life [3], [4], [5], [6].
The percentage of fetuses with FGR due to (relative) uteroplacental dysfunction and/or
concomitant relative maternal heart failure increases particularly in late and prolonged
pregnancy, and this is associated with a corresponding perinatal risk [7].
Apart from the timely diagnosis and identification of the causes of FGR, the obstetric
challenge primarily entails continued antenatal management with optimum timing of
delivery. Intensive fetal monitoring aims to prolong the pregnancy in order to minimise
preterm morbidity, and at the same time to intervene, i.e. deliver, before the fetus
is threatened or harmed. This review summarises the current recommendations of the
German AWMF guideline 015/080 “Intrauterine Growth Restriction” [1].
Definitions
The definitions of constitutionally small fetuses and those with fetal growth restriction
in international guidelines and literature vary greatly [8]. In particular, the terms “small for gestational age” (SGA) and FGR must be differentiated
with regard to content and thus clinical management. In line with the guidelines,
this review uses the terms SGA and FGR (IUGR) solely in terms of fetal growth and
does not consider any other fetal conditions.
SGA fetuses consistently demonstrate growth rates below the 10th percentile [1]. In many cases this is more a reflection of constitutional factors such as gender,
parental height and ethnicity and is usually not linked to a medical condition. SGA
fetuses continue to grow linearly and do not exhibit other parameters of fetal distress
(e.g., oligohydramnios or Doppler abnormalities); however, it should be noted that
the lower the percentile, the higher the morbidity and mortality risk: SGA fetuses
with growth below the 3rd percentile have a significantly higher morbidity and mortality
risk despite constant percentile growth [9].
SGA fetus must be differentiated from FGR, since in the latter cases the fetus does
not realise its genetically determined growth potential. This results in the typical
flattened growth curve, i.e., a “crossing of centiles”. Often FGR fetuses also demonstrate
growth below the 10th percentile, i.e., they are “small for gestational age”, but
a flattened growth curve (and thus FGR) may also appear in fetuses with an estimated
weight above the 10th percentile, especially in third trimester late-onset FGR.
FGR is one of the most common causes of obstetric complications with unfavourable
perinatal and neonatal outcome, particularly in the context of prematurity. The fetuses
in question exhibit a higher prevalence of poor long-term neurological development
as well as cardiovascular and endocrinological disorders [3], [4], [5], [6]. Almost 30 – 50% of all intrauterine deaths are related to FGR [10].
According to current expert opinion, fetal abdominal circumference or estimated fetal
weight < 3rd percentile and abnormal indices of the umbilical artery are decisive
parameters for the definition of early-onset or late-onset FGR [11]. According to the current German guideline, the following definitions apply to SGA
and FGR (see box) [1]:
Definition
SGA/FGR definition according to AWMF Guideline 015/080
SGA
FGR
-
Estimated fetal weight < 10th percentile and/or
-
“crossing of centiles” growth and
-
Abnormal umbilical artery Doppler ultrasound or
-
Abnormal uterine artery Doppler ultrasound or
-
Oligohydramnios
Aetiology and Epidemiology
Aetiology and Epidemiology
The pathogenesis of fetal hypotrophy includes maternal, fetal and placental factors
([Table 1]) [1]. In many cases, the different underlying pathophysiological mechanisms ultimately
culminate in placental failure, which occurs as a result of unsuitable transformation
of the maternal spiral arteries due to inadequate invasion of extravillous trophoblasts
and thus deficient uterine perfusion. This leads to placental hypoxia with secondary
injury to the villous architecture [12].
Table 1 Causes and risk factors of fetal growth restriction (according to [1]).
|
Origin
|
Causes and risk factors
|
|
Maternal
|
-
Preexisting diseases (e.g., diabetes, hypertension, cardiac disorder, renal disorder,
autoimmune disorder (antiphospholipid syndrome, systemic lupus erythematosus), chronic
respiratory disorder, severe anaemia)
-
Hypertensive disorders of pregnancy, pre-eclampsia
-
Prior FGR (either previous pregnancy or maternal FGR)
-
Substance abuse (nicotine, alcohol, drugs)
-
Low socio-economic status
-
Infertility treatment
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Weight (increased or very low body mass index)
-
Age (< 16 years; ≥ 35 years)
-
Embryo-/fetotoxic drugs and teratogens
|
|
Fetal
|
|
|
Placental
|
-
Abnormal placentation
-
Placental infarctions
-
Chronic placental abruption
-
Umbilical cord pathology (velamentous insertion, single umbilical artery)
-
Placental mosaic
-
Placental tumours
|
Diagnostic Work-up
Prenatal management according to the maternity guidelines includes regular monitoring
of the fundal height. Since the available clinical examinations can only provide limited
information, the diagnostic work-up should be extended (initially by ultrasound) in
case of abnormalities, i.e., “abdominal circumference too small/fundal height too
low”. [Fig. 1] summarises the examination algorithm in suspected SGA/FGR.
Fig. 1 Diagnostic examination algorithm in suspected SGA/FGR.
Checking the gestational age
The diagnosis of FGR includes the most accurate assessment of the gestational age
possible. Ideally, this is based on the crown-rump length (CRL) in the first trimester.
This parameter provides the most reliable information [13]; in case of discrepancies in an otherwise unremarkable embryo, the (anamnestic)
gestational age should be corrected by ultrasound, if it differs by at least 7 days
from the age determined by ultrasonography – unless the date of conception is definitely
known (e.g. IVF/ICSI) [1].
If CRL measurements are not available (e.g., if pregnancy is diagnosed late), the
gestational age may also be estimated from the biparietal or transcerebellar diameter.
A discrepancy between the gestational age calculated based on the last period and
according to ultrasound may be the first sign of an early developmental disorder.
Such cases call for further assessment and intensive monitoring.
Fetometry
Apart from estimated weight, fetal abdominal circumference is the most important indicator
of impaired fetal growth. Fetal weight can be determined with the Hadlock formula,
which is recommended in increased risk of FGR [1]. It should be noted that parental characteristics need to be taken into account
when estimating weight.
According to the definition of FGR, assessment should include not only the current
estimated weight, but also the growth curve in order to detect flattening of the latter,
especially since FGR is not limited to weights below the 10th percentile.
Amniotic fluid
Amniotic fluid volume is often reduced in FGR, as this disorder can be accompanied
by fetal oliguria. But usually the amniotic fluid volume is unremarkable [1], [14]. Evaluation of the amniotic fluid volume may be based on the “single deepest pocket”
(SDP) technique or measurement of the amniotic fluid index (AFI) [15], with the SDP appearing to be more useful in predicting adverse outcome [16].
If the suspected diagnosis of SGA/FGR is confirmed, this should be followed by further
evaluation of the causes and assessment of the fetal condition. This includes Doppler
ultrasound assessment of the uteroplacental unit (uterine and umbilical arteries)
and possibly other fetal vessels (middle cerebral artery, ductus venosus), as well
as detailed diagnostic ultrasonography. In addition, differential diagnosis may profit
from genetic assessment of any chromosomal pathology and/or fetal infection when planning
the subsequent management [1].
Detailed diagnostic ultrasonography
Differential diagnostic assessment of possible FGR calls for further differentiated
diagnostic organ work-up (along the lines of the German DEGUM II criteria) ([Fig. 1]) [1]. It should be noted that structural abnormalities of the fetus are indicative of
genetic-syndromal diseases, especially in early-onset and multiple pathologies [17]. At least the genetic analysis should be offered.
Doppler ultrasound
Doppler ultrasound is mandatory in suspected SGA/FGR, not only for the differential
diagnosis of SGA/FGR, but also for determining the cause of the FGR. Higher indices
in the uterine and umbilical arteries indicate placental disorder along the lines
of placental failure. When diagnosing FGR, other fetal vessels (middle cerebral artery,
ductus venosus) should be examined as well to evaluate the fetal condition [1].
Screening, Prediction and Prevention
Screening, Prediction and Prevention
At present, there is no screening approach available combining good sensitivity and
specificity with negative or positive predictive value [18].Similar to the first-trimester risk evaluation in pre-eclampsia, screening for fetal
growth restriction can be performed by combining the maternal medical history, Doppler
ultrasound of the uterine arteries, mean arterial blood pressure, and the biochemical
marker PAPP-A [19]. Even if the detection rate does not match that of pre-eclampsia screening, it can
be used to detect some pregnancies with a high risk of FGR which will then be closely
monitored.
In the second trimester Doppler ultrasound of the uterine arteries in low-risk cohorts
is only of limited use, while in a cohort at risk it offers a moderate predictive
benefit for early detection of FGR [20]. Therefore, Doppler ultrasound of the uterine arteries when screening for FGR is
regarded as somewhat under discussion [21]. However, abnormal findings should prompt regular ultrasound studies of growth and
Doppler checks (uterine and umbilical arteries).
The combination of Doppler ultrasound and angiogenic factors (e.g., sFlt-1/PlGF ratio)
appears to improve the FGR prediction, as does the combination of fetal biometry and
the angiogenic marker [22], [23], [24]. However, further studies are still needed before widespread clinical use.
Antenatal diagnosis of FGR is essential, since this has a positive effect not only
on the course of pregnancy but also on neonatal outcome [2], [25]. Despite closely monitored management internationally and also in Germany, the number
of unidentified antenatal FGR cases is still large [1], [25].
According to maternity guidelines, fetometry is performed between 18 + 0 and 21 + 6
wks and 28 + 0 and 31 + 6 wks. This approach detects early-onset FGR quite well, but
does not identify the majority of late-onset growth restrictions (approx. 70 – 80%
of FGR), particularly if no Doppler ultrasound evaluation or subsequent biometry is
performed.
In order to improve this situation, the definition of FGR requires that the assessment
should include not only the current estimated weight, but also the growth curve in
order to detect flattening of the latter, especially since FGR is not limited to weights
below the 10th percentile. In case of irregularities, further studies, i.e., repeat
biometry, Doppler ultrasound and possibly measurement of the angiogenic markers could
be performed [26]. This is particularly important, since early/correct diagnosis of FGR can reduce
the perinatal risk [27].
An (additional) late biometry at ≥ 36 wks improves the FGR detection rate by a factor
of 3 [28], [29]. Combined with the assessment of fetal growth over time it is possible to detect
a subgroup with high perinatal risk [28], [30]. Pathologies on Doppler ultrasound (maternal, fetoplacental or fetal) correlate
with less favourable perinatal outcome [27], [31], [32]. 15 – 20% of cases with late-onset FGR exhibit abnormal cerebral perfusion – with
unremarkable blood flow in the umbilical cord; by determining the cerebroplacental
ratio (CPR) fetuses (with and without growth problems) at increased risk of unfavourable
perinatal outcome can be detected more easily [33], [34], [35]. The combination of biometry, uterine Doppler ultrasound and CPR in the third trimester
can detect the majority of fetuses with a high risk of intrauterine fetal death (IUFT)
[31], but appears to be of little help in detecting SGA/FGR in non-selected populations
[36]. The combination of fetal biometry and measurement of angiogenic factors (especially
the sFlt-1/PlGF ratio) also seems to be useful in FGR detection [23], [37], [38].
Unlike in pre-eclampsia, the administration of low-dose aspirin appears to be only
moderately successful in the prevention of FGR (although the trial did not have enough
statistical power for the prevention of FGR) [39]; this also requires further studies. The results of the German multicentre trial
on the benefit of NO-donor PETN in women with pathological Doppler ultrasound of the
uterine arteries in the second trimester are expected soon [40].
SGA/FGR Management
FGR management is a challenge for all involved: Fetal hypoxemia should be diagnosed
early to avoid irreversible damage and intrauterine death. On the other hand, in order
to minimise the sequelae of prematurity pregnancy should not be terminated too early.
Parents must be involved in all decisions and the consequences of the different options
must be explained to them. In particular, the increased risk of intrauterine fetal
death under “watchful waiting” must be contrasted with the increased mortality and
morbidity risk of prematurity at delivery. Thus, close antenatal and perinatal cooperation
with the neonatologists is necessary to provide the parents with adequate information.
It is important to note that early-onset FGR should be assessed differently than late-onset
FGR. In early-onset FGR progressive deterioration is reflected in abnormal venous
Doppler parameters, while in late-onset FGR this manifests primarily in cerebral Doppler
sonography ([Table 2]) [1], [41].
Table 2 Early-/late-onset FGR (according to [42]).
|
Early-onset FGR (< 32 + 0 wks – 1 – 2%)
|
Late-onset FGR (≥ 32 + 0 wks – 3 – 5%)
|
|
Problem: Management
|
Problem: Diagnosis
|
|
Placental failure: major (abnormal fetoplacental perfusion, high correlation with
pre-eclampsia)
|
Placental failure: minor (often normal fetoplacental perfusion, low correlation with
pre-eclampsia)
|
|
Hypoxia ++: systemic cardiovascular adaptation
|
Hypoxia ±: central cardiovascular adaptation (“brain sparing”)
|
|
Fetal immaturity → higher hypoxia tolerance → longer course possible
|
Fetal maturity → low hypoxia tolerance → no (or very short) course
|
|
High morbidity and mortality, low prevalence
|
Low mortality (but main cause of IUFT), poor long-term outcome, higher prevalence
|
No individual monitoring approach can predict the outcome of FGR in valid fashion;
a combination of different approaches is recommended. In order to improve the perinatal
outcome, FGR monitoring requires in particular ultrasonography and above all Doppler
ultrasound.
Management of pregnancies with SGA or FGR fetuses relies on a combination of different
examination techniques, which are summarised in [Fig. 2]
[1]. Monitoring of fetal growth, amniotic fluid volume, and arterial and venous fetal
vessels is mandatory; CTG/computerised CTG monitoring also provides important information
on the fetal condition [1], [42].
Fig. 2 Management protocol in fetal growth restriction (data from [1]).
Biometric monitoring
Serial ultrasound monitoring of fetal growth is essential in the management of fetuses
with SGA/FGR. However, it should be noted that – also due to the limitations of weight
estimation by ultrasonography – the intervals between examinations should not be too
short: the interval between such examinations should be at least 2, preferably 3 weeks
[1], [43].
Doppler ultrasound
-
Umbilical artery: Doppler ultrasound of the umbilical arteries permits haemodynamic changes to be detected
in the course of the disease. In FGR normal resistance ratios also indicate a low
risk of unfavourable perinatal outcome and low perinatal mortality [9]. The prognosis worsens depending on the degree of increase in resistance [41]. In so-called ARED flow (absent/reversed end-diastolic flow) about 70% of the placental
vessels are occluded [44], which in “reversed end-diastolic flow” increases the risk of perinatal mortality
by a factor of 5. [Fig. 2] lists the recommended study intervals based on studies of progressive Doppler deterioration
[45]. If the resistance in the umbilical arteries is unremarkable, two-week intervals
appear to be adequate [46].
-
Ductus venosus: In the care of early-onset FGR the ductus venosus is a key vessel [41], and management of early-onset FGR should base its assessment on the evaluation
of this vessel [1]. Changes in the venous circulation including reversed blood flow usually appear
later than changes in the arterial system [41]. Pathophysiologically, increasing cardiac dysfunction results in decreased diastolic
blood flow or increased pulsatility in the ductus venosus including loss of the positive
a-wave; absent a-wave or reverse blood flow is an indication of cardiovascular instability
and may be a sign of imminent or already present acidemia [47], [48], [49], with the risk of intrauterine death doubling daily [45], [47].
-
Middle cerebral artery: Examination of the middle cerebral artery (MCA) can detect progressive hypoxaemia,
since the increasing fetal compromise leads to a redistribution of blood (“brain-sparing
effect”) [41]. MCA resistance decreases and is considered abnormal for a pulsatility index (PI)
< 5th percentile [1]. While in early-onset FGR the predictive power of the MCA is limited with regard
to predicting unfavourable perinatal outcome [50], [51], [52], the examination of the MCA, preferably when combined with examination of the umbilical
artery as the so-called cerebroplacental ratio (CPR), gains importance in the management
of late-onset FGR. On the one hand, CPR allows a more precise diagnosis of late-onset
FGR [42], while various studies have demonstrated a benefit
in predicting unfavourable perinatal outcomes in pathological CPR, i.e., ratios
between umbilical artery and and middle cerebral artery (< 5th percentile or < 1)
[53], [54], [55], [56].
(Computerised) Cardiotocography (cCTG)
According to maternity guidelines cardiotocography (CTG) should always be performed
as part of prenatal care if placental insufficiency is suspected [1]. However, it detects acute rather than chronic courses [41] and therefore should never be the sole monitoring technique when managing FGR [1].
To minimize the limitations of a CTG examination (subjective assessment), a computer-based
analysis of the CTG can be employed. Major benefits of this technique include the
higher degree of objectivity of the assessment as well as the option of analysing
the short-term variation (STV) [57]. As in uncomplicated pregnancies, the STV increases with gestational age in FGR,
but the STV values are generally lower [58]. An STV of 4.5 ms rules out fetal acidemia (NPV 100%) [59], while decreasing STV values are associated with earlier delivery, lower birth weight,
lower pH of the umbilical artery, poorer acid-base status and worse neonatal outcome
[60].
Measuring the STV and observing its course over time may detect subtle changes, which
can be helpful for better timing of the delivery [61], thus underlining the use of this measure in FGR management; nevertheless, it must
be taken into account that CTG changes in FGR only manifest themselves rather late
[41], [61], and that the short-term variation is also affected by medication (e.g., with antenatal
corticosteroids), which must therefore be considered when interpreting the results
[1], [62], [63].
Other Measures
Inpatient/outpatient management
In general, surveillance of pregnancies with FGR may be performed in an outpatient
setting, as there is no evidence-based data on which to base indications for inpatient
monitoring. With increasing severity and fetal impairment, however, inpatient monitoring
can be helpful if close intervals between examinations become necessary. The link
between early-onset FGR and pre-eclampsia should also be noted. The decision for outpatient
or inpatient care should be made on a case by case basis [1].
Antenatal corticosteroid administration
One challenge in obstetrics (and thus also in the management of FGR) is in estimating
the time of expected delivery in the preterm setting. If delivery is expected within
the next 7 days, corticosteroids should be administered [1], [64]. The benefits of antenatal corticosteroids are also seen in growth-restricted fetuses.
It should be noted, however, that corticosteroid administration may temporarily reduce
heart rate variation as well as fetal body and respiratory movements; these changes
normalise within 72 hours [1].
In addition to the “timing” of steroid administration noted above, it generally is
true that non-critical administration of steroids should not be undertaken in all
FGRs, since corticosteroids – in addition to their undisputed positive benefits –
also have various negative effects (including reduced growth, delayed neurological
development, stress, hypertension). In addition, fetuses with FGR, especially with
increasing hypoxaemia, already possess high cortisol levels, and after 30 wks fetuses
with FGR develop RDS much less often than eutrophic fetuses. There is insufficient
data on the effect of steroids on long-term outcome in fetuses > 30 wks with FGR.
Therefore, the goal should be to avoid as much as possible antenatal steroid application,
especially repeated courses in women who in the end do not give premature birth [65].
Magnesium for fetal neuroprotection
The antenatal intravenous administration of magnesium appears to have a neuroprotective
effect and thus may help to reduce the risk of neurological damage. Since FGR correlates
with an increased risk of fetal prematurity, (inter)national medical societies recommend
the administration of magnesium sulphate before 32 + 0 wks for neuroprotection when
birth is imminent [1], [64].
Birth/Delivery in SGA/FGR
Birth/Delivery in SGA/FGR
Place of delivery
In order to ensure immediate and continuous care in the FGR setting, delivery should
proceed in a perinatal centre with neonatal intensive care unit and an experienced
paediatric team [1].
Time of delivery
When planning the timing of delivery, the risks of preterm delivery must be weighed
against those of continuing the pregnancy and/or the maternal risks. Maternal delivery
criteria apply regardless of the gestational age and extent of the FGR.
In terms of the fetus, the timing of delivery is governed not only by the gestational
age but also the Doppler ultrasound findings ([Fig. 2]). As noted above, early-onset FGR is accompanied by a serious deterioration, particularly
in venous abnormalities (ductus venosus), while late-onset FGR is associated with
cerebral vascular disorders (ACM, CPR). This is reflected in the recommendations of
(inter)national guidelines and experts [1], [42], [66], [67].
Note: Just like decelerations, the cut-off values (cCTG and ductus venosus) given below
are late signs of fetal deterioration. Some of these cases may already suffer from
myocardial dysfunction and possibly hypotension, and the fetal adaptation mechanisms
no longer fulfil their protective function. This implies that the significance of
these parameters diminishes with increasing gestational age.
-
cCTG: In case of new-onset CTG pathologies (recurrent, unprovoked, and refractory decelerations
at any time) delivery should be considered [1], [61]. Delivery should be considered if STV is < 2.6 ms at 26 + 0 to 28 + 6 wks and < 3.0 ms
at 29 + 0 to 32 + 0 wks ([Fig. 2]) [1], [61].
-
Ductus venosus (early-onset FGR): According to current knowledge, pathological findings of the ductus venosus may be
an indication for delivery if the fetus is viable and antenatal corticosteroids have
been administered [1]. Depending on the gestational age and possible additional findings, delivery should
be discussed with the expectant mother in case of increased resistance (> 95th percentile
– accompanied by a decreased a-wave); in case of absent or reverse a-waves delivery
is indicated [1], [41], [42], [61], [66].
According to our current understanding, the combination of computerised CTG and ductus
venosus is the “optimum” approach for monitoring early-onset FGR [68]. If Doppler ultrasound of the ductus venosus is unremarkable and in the absence
of cCTG pathology, it may nevertheless be appropriate to terminate the pregnancy earlier.
-
Umbilical artery: With absent or reversed end-diastolic flow (AREDF) in the umbilical artery the prognosis
can be poor [1], [41], [69], but the morbidity and mortality associated with preterm birth before 32 + 0 wks
is also rather high [70], while continued pregnancy offers clear benefits in outcome [71]. Taking this into account, for ARED-flow the current guideline recommends: In REDF,
delivery may be considered from 30 + 0 wks and should be performed at 32 + 0 wks.
In absent end-diastolic flow (AEDF) the mortality risk is lower, but delivery should
be performed at 34 + 0 wks [1]. In an otherwise unremarkable course, waiting until these weeks of pregnancy is
possible and after two years does not result in any significant differences in morbidity
and mortality [72]. Increased resistance in the umbilical artery (PI > 95th percentile) is also linked
to increased risk in perinatal morbidity and mortality, but with low predictive power.
With increased PI > 95th percentile, delivery is therefore recommended from 37 + 0
wks [1].
-
Middle cerebral artery/cerebroplacental ratio: In the preterm setting (< 37 + 0 wks), the prognostic power of the MCA is of limited
use in predicting acidemia and poor perinatal outcome, and should not be used to determine
delivery timing at this stage [1]. Delivery should be considered starting at 37 + 0 wks if resistance in the MCA is
low (PI < 5th percentile) [1]. At present, the cerebroplacental ratio (CPR) is still under contention, since precise
limits in particular have not been clearly evaluated yet. Since some studies have
shown that an abnormally low CPR is a predictor of poor perinatal outcome, delivery
can be considered from 37 + 0 wks [1].
Since fetuses with isolated SGA, i.e. fetal growth < 10th percentile, unremarkable
Doppler findings and no additional risks, have an increased risk of intrauterine death,
despite a generally favourable outcome, earlier delivery from 38 + 0 wks may be considered
in SGA fetuses as well. In fetuses with isolated SGA prolonged pregnancy should be
avoided [1], because ultimately SGA and GFR cannot be reliably differentiated with current techniques
of fetal monitoring (biometry, utero-umbilico-fetal Doppler, BPS, NST) in all cases,
and relative uteroplacental failure is increasingly seen close to the expected date
of delivery.
When Doppler ultrasound and cCTG are unremarkable, isolated growth arrest is not an
independent factor for immediate termination of pregnancy. These constellations should
always consider the gestational age and the measurement interval should be checked
in order to minimise the systematic error when estimating the weight by ultrasonography
[1].
Type of delivery
In addition to gestational age, parity and cervical maturation, various other factors
such as the presence of abnormal findings (Doppler, cCTG) and other fetal or maternal
specifics or complications must be taken into account when deciding on the type of
delivery, and this decision must be made for each patient individually [1]:
In FGR with unremarkable Doppler findings or increased pulsatility in the umbilical
artery (> 95th percentile) – not with ARED flow – labour can be induced and vaginal
delivery attempted. However, the higher risk of complications must be taken into account
mandating continuous intrapartum monitoring [1].
In abnormal Doppler findings such as increased resistance in the umbilical artery
(not ARED flow) and in late-onset FGR with abnormal ACM/CPR values, induction of labour
and vaginal delivery are possible, with continuous intrapartum monitoring mandatory
[1].
In early-onset FGR with pathological cCTG, abnormal ductus venosus and/or especially
in ARED-flow, caesarean section is usually recommended and performed, if only because
of the increasingly impaired fetal condition that this situation signifies. Also in
very early weeks of pregnancy caesarean section must be performed if the termination
of pregnancy is indicated and when there is no meaningful option to induce delivery
[1].
