Managing fetal growth disorders
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Managing fetal growth disorders
- 2. Defining disorders of growth requires relating a given achieved growth to an expected growth. Within genetically set limits, the actual fetal growth judged by Fetal weight is determined by the - genetic growth potential which varies from race to race and individual to individual , - the health of the fetus with good fetal circulation, - the capacity of the mother to supply adequate quality and quantities of substrates ( O2 , glucose, aminoacids etc) required for growth,
- 3. ď˝ With a prevalence of the 5â8% in the general population, IUGR can complicate 10% to 15% of all pregnancies . - However, only 20â30% of these fetuses are small because of a pathological restriction of their growth (PFGR) and a majority are normal SGA -IUGR represents the second cause of perinatal mortality, after prematurity -It is related to an increased risk of perinatal complication as hypoxemia, low Apgar scores, and cord blood acidemia, with possible negative effects for neonatal outcome. -It is associated with increased risk of neurological, cardiovascular and metabolic
- 4. In practice, due to error in estimating gestational age, inaccuracy in weight estimation, and variation in true genetic potential, there will be no cut off that correctly separates normal and abnormal IMPORTANT TERMS IN FETAL GROWTH DISORDER SGA simply refers to a weight for gestation below a given threshold, but a significant proportion of smallness is due to constitutional or physiological causes, The most commonly used definition of SGA is a birth weight below the 10th percentile for gestational age. IUGR SIGNIFIES THE PATHOLOGICAL CAUSE OF SAME CUTOFF
- 5. Endocrine regulation of fetal growth â IGF -1 IGF -2 Placental regulation of fetal growth â Implantation and early placentation play crucial role Genomic imprinting and fetal growth
- 6. -Placental insufficiency 75â80% -Maternal conditions not associated with placental insufficiency 5% -Fetal chromosome abnormalities 5% -Multifactorial fetal abnormalities 2â3% -Fetal infections 1%
- 7. 1. Associated with placental vascular insufficiency: -Preeclampsia -Chronic hypertension - Chronic renal disease - Connective tissue disorder -Diabetes with vascular lesions -Sickle cell anemia -Cardiac disease class III or IV -Multiple gestation -Autoimmune diseases, including: APS -Genetic disorders, including: phenylketonuria. 2. Not associated with placental insufficiency -Severe malnutrition -Smoking -Alcohol ingestion and recreational drugs -Hemoglobinopathies
- 8. Alterations in the uteroplacental and fetalâplacental circulations ⢠Abnormal trophoblast invasion: ⢠pre-eclampsia ⢠placenta accreta. ⢠Infarction ,villitis , hemorragic endovasculitis, ⢠Abruption ⢠Placental location: placenta praevia. ⢠Tumours: chorioangiomas ,placental haemangiomas ⢠Abnormal umbilical cord or cord insertion: two-
- 9. Lack of substrate and inability to reach genetic potential ⢠Genetic abnormalities, including: ⢠trisomy 13, 18, or 21 ⢠turnerâs syndrome ⢠triploidy. ⢠Congenital abnormalities, including: ⢠cardiac, e.g. TOF, transposition of the great vessels ⢠gastroschisis. ⢠Congenital infection, including: ⢠CMV ⢠rubella ⢠toxoplasmosis. ⢠Multiple pregnancy
- 10. -Type I or symmetric FGR corresponds to fetuses that are symmetrically small and have normal H/A and F/A ratios. Type II or asymmetric FGR corresponds to fetuses that have an AC that is smaller than the HC and the FL resulting in abnormally high H/A and F/A ratios. Type III or intermediate FGR corresponds to fetuses that are initially symmetric but become asymmetric later in the pregnancy.
- 11. âIntrinsicâ- FGR occurs when the fetuses are small due to fetal conditions such as viral infections or chromosomal abnormalities. âExtrinsicâ -FGR occurs when the growth failure is due to an element outside of the fetus such as a placental condition or a maternal disease. âCombinedâ- FGR occurs when there are extrinsic and intrinsic factors causing the growth failure and âIdiopathicâ -FGR when the cause of the fetal
- 12. BASED ON DOPPLER FINDINGS NOT BIRTHWEIGHT SOLELY 1) Small for gestational age (SGA) refers to those small fetuses with no discernible pathology and with normal umbilical artery and middle cerebral artery Doppler results; 2) Growth-restriction refers to small fetuses with recognizable pathology and abnormal Doppler studies; and 3) Idiopathic growth restriction applies to small fetuses with no discernable pathology and abnormal Doppler studies.28
- 13. ď˝ Early-onset FGR represents 20â30% of all FGR and is associated with gestational hypertension and/or pre-eclampsia in up to 70%. Late-onset FGR, which represents approximately 70â80% of cases of FGR, shows a weaker association with hypertensive disorders of the pregnancy, roughly 10%
- 16. 1) Maternal socio-economic condition and nutritional status 2) Maternal smoking , alcohol intake , teratogen intake or substance abuse in past and present 3) Previous history of growth restriction or still birth - 50% increased risk of severe growth restriction - Stillbirths before 32 weeksâ gestation have a particularly strong association with IUGR. 4) Medical disorders 5) Diabetes -Preeclampsia is observed in 15-20% of pregnancies complicated by type 1 diabetes mellitus without nephropathy and approximately 50% in the presence of nephropathy. 6) Low PAPP-A , two vessel cord and multiple pregnancy 7) IVF pregnancy
- 17. Biochemical markers. In the first trimester, an unexplained low pregnancy-associated plasma protein A or human chorionic gonadotropin (hCG) is associated with an increased risk of placental-related diseases such as IUGR or preeclampsia. Early growth restriction. Low first-trimester measurement of crown-rump length in pregnancies dated by the last menstrual period is also linked with FGR. Slow growth between the first and second trimester is able to identify a subgroup of slow-growing babies that are at increased risk of perinatal death before 34 weeksâ gestation, in most cases with growth restriction.
- 18. Biochemical markers - an unexplained elevation of serum alpha-fetoprotein, hCG, or inhibin-A is also associated with these adverse outcomes. Uterine artery Dopplers -. Uterine Doppler evaluation in the second or first trimester has been proposed as a screening tool for early-onset IUGR,with detection rates of about 75% and 25%, respectively, for a false-positive rate of 5-10%. These sensitivities are higher for predicting early IUGR associated with preeclampsia and lower for late IUGR. SCREENING IN SECOND TRIMESTER Different strategies combining maternal risk factors, blood pressure, and biochemical markers have been published with detection rates greater than 90% for early-onset preeclampsia and associated IUGR
- 19. Serial fundal height assessment Routine/intermittent third-trimester ultrasound biometry Serial ultrasound biometry. For pregnancies at risk due to past or current situation , serial assessment of estimated fetal weight or abdominal circumference is the best predictor of FGR as assessed by neonatal morphometry. Therefore, serial biometry is the recommended gold standard
- 20. Serial ultrasound biometry. For pregnancies at risk, serial assessment of estimated fetal weight or abdominal circumference is the best predictor of FGR as assessed by neonatal morphometry Amniotic fluid. A metaanalysis 132 of 18 randomized studies demonstrated that an amniotic fluid index of less than 5 is associated with abnormal 5 minute Apgar score but failed to demonstrate an association with acidosis. Longitudinal studies in early-onset IUGR fetuses have shown that the amniotic fluid index progressively Routine/intermittent third-trimester ultrasound biometry. Sensitivity of AC for detecting a birthweight less than the 10th centile ranges from 48% to 87%, with specificity from 69% to 85%. For estimated fetal weight, sensitivities of 25- 100% have been reported, with a specificity of 69-97%.
- 21. First, the standard is customized for sex as well as maternal characteristics such as height, weight, parity, and ethnic origin based on-one size does not fit all theory. Second, pathological factors such as smoking, hypertension, diabetes, and preterm delivery are excluded to predict the optimum weight that a baby can reach at the end of a normal pregnancy. Third, the term optimal weight and associated normal range is projected backward for all gestational age points, using an ultrasound growth based proportionality curve It is calculated by computer software CUSTOMISED GROWTH CHART â THREE PRINCIPLES
- 23. CARDIOTOCOGRAPHY
- 24. For the practicing obstetrician, these problems can be summarized in following five important questions: ?? How to recognize that the fetus is small ?? How to differentiate between the fetuses that are small and healthy and the fetuses that have pathological growth restriction? ?? Which is the appropriate fetal surveillance method and follow up interval ? ?? How to manage the pregnancies afflicted by pathological fetal growth restriction (PFGR) as per their staging of deterioration ? ?? How to optimize the timing and mode of
- 40. ANTEPARTUM COMPLICATIONS are an increased incidence of stillbirth, oligohydramnios, and antepartum fetal distress. INTRAPARTUM COMPLICATIONS are fetal hypoxia, acidosis, and high rate of cesarean delivery. NEONATAL COMPLICATIONS are multiple and include hypoglycemia, hyperbilirubinemia, meconium aspiration, persistent fetal circulation, hypoxic-ischemic encephalopathy, hypocalcemia,
- 41. OXYGEN â No role PLASMAVOLUME EXPANDERS â no role BETA MIMETICS - Larger, well-designed studies are needed to evaluate the effects of betamimetics on fetal growth. Since there is potential for adverse effects due to the pharmacological characteristics of this group of drugs BED REST IN HOSPITAL- There is not enough evidence to evaluate the use of a bed rest in hospital policy for women with suspected impaired fetal growth. AMNIOINFUSION - Amnioinfusion with saline solution should be one of the initial steps in the intrapartum management of the PFGR fetus with decreased amniotic fluid volume or early MSL. SILDENAFIL ( NO promoter ) â Phosphodiesterase inhibitors. The enzyme phosphodiesterase breaks down cGMP, an enzyme critical to the effect of NO. But sildenafil
- 42. - Always determine the correct gestational age . - Patients with high-risk factors, unreliable dates, and abnormal or difficult to assess uterine growth are at risk for carrying small fetuses. -In the majority of cases the clinical findings and ultrasound measurements allow only the diagnosis of âsmall fetus.â The majority of small fetuses are healthy. Only a modest proportion of small fetuses are truly undernourished or PFGR. - To distinguish between fetuses that are small and healthy and PFGR it is necessary to use serial growth charts and Doppler assessment of the uterine, umbilical, and mid cerebral artery resistance.Dopplers are not only diagnostic
- 43. - Uterine artery, UA, and MCA Doppler do not identify all PFGR fetuses. Doppler technology is exclusively for the identification of PFGR because of placental insufficiency. Small fetal size in the presence of normal uterine, umbilical, and midcerebral Doppler rules out placental insufficiency . - The most important surveillance tests to follow the PFGR fetus are the FHR monitoring by CTG and the umbilical and cerebral Doppler. As long as the FHR monitoring is normal and the Doppler does not show fetal decompensation (ADF or RDF) expectant management is adequate. - The placentas of all PFGR babies should be examined by a competent placental pathologist. In many cases the placenta will provide evidence regarding the etiology of the problem. -The earlier in gestation IUGR is detected, the greater the possibility of developmental problems later in life. The
- 45. Staging system and management ¡ Stage 0 SGA fetuses have a good prognosis. They are managed as outpatient with Doppler assessment every 2 weeks. If the Doppler remains normal, delivery is recommended at term. If the Doppler becomes abnormal, these fetuses are managed as Stage I IUGR fetuses. ¡ Stage I IUGR fetuses are considered to have mild growth restriction, and affected mothers who are without preeclampsia are usually managed as outpatients. Antenatal corticosteroids should be given at time of diagnosis. In these fetuses, twice-weekly antenatal testing is recommended. If the non-stress testing (NST) remains reactive and the AFI remains >5.0 cm, delivery is recommended at 37 weeksâ gestation. If the umbilical artery Doppler becomes absent, these fetuses should be managed as Stage II IUGR. ¡ Stage II IUGR fetuses should be managed as inpatients. During hospital admission, the fetuses should undergo daily antenatal testing with twice-daily NST and daily biophysical profile (BPP). If the NST remains reassuring and the BPP score remains between 6 and 8 of 8, continuation of expectant management is recommended. In addition, antenatal corticosteroids should be given at time of diagnosis. Delivery is recommended at 34 weeks. If any of the aforementioned NSTs become non-reassuring or if the BPP score is 4 of 8 on 2 occasions at least 4 hours apart, immediate delivery is recommended. Delivery should occur via cesarean delivery because fetuses with an absent/reversed flow of the umbilical artery will not tolerate labor induction. ¡ Stage III IUGR fetuses are managed the same as Stage II except for delivery at 32 weeksâ gestation, regardless of gestational age at time of diagnosis. As with Stage I and II, antenatal corticosteroids should be given at time of diagnosis. The advantage of the above scoring system is its simplicity. Only fetal biometry, sonographic interrogation of three fetal vessels, and the amniotic fluid index are needed. It also allows classification of all small fetuses. Of note is that if the umbilical artery and middle cerebral artery Doppler is normal, it is determination of flow velocity waveforms of the ductus venosus is unnecessary because it will be normal as well. The presence of IUGR in the setting of preeclampsia should not deter standard management of preeclampsia. It is important to note the rate of mortality in the staging system.29 No deaths occurred in Stage 0 or Stage I fetuses, whereas the mortality for stage III fetuses is high (50% if there was reversal of flow in the ductus venosus; 85% mortality was observed when reversal of flow in the ductus venosus was present in combination with one of the other parameters that characterize stage III), whereas the mortality in stage II IUGR fetuses was intermediate between stages I and III (Figure 4). Also, studies have shown that fetuses can survive for days or weeks with reversal of flow in the ductus venosus.29 A recent preliminary study reported that fetuses with reversal of flow in the ductus venosus will not necessarily be acidemic at birth.30 In addition, the majority of affected pregnancies have an AFI <5 cm before
Hinweis der Redaktion
- Fetal weight is determined by the genetic growth potential, the health of the fetus, the capacity of the mother to supply adequate quality and quantities of substrates required for growth, and the ability of the placenta to transport these nutritional substrates to the fetus. The genetic growth potential varies from race to race and from individual to individual and this variation is evident in population studies of healthy term newborns showing a symmetrical distribution curve of their birth weights. Normal fetuses at either extreme of this normal biological distribution curve will be combined with others whose growth has been restricted or accelerated due to pathological influences The most important are oxygen, glucose, and amino acids. Oxygen crosses the placenta by simple diffusion and is necessary for the formation of chemical energy in the form of adenosine triphosphate (ATP). Glucose crosses the placenta by facilitated diffusion and its concentration in the fetusis determined by the maternal plasma glucose levels.Glucose is utilized in the production of energy and in the provision of carbon-building blocks for the synthesis of lipids, glycogen, nucleotides, and other molecules. Amino acids cross the placenta by active transport and are essential for the synthesis of proteins. Any persistent decrease in the availability of these substrates will limit the ability ofthe fetus to reach his/her growth potential, and a severe substrate deficiency may threaten the ability of the fetus to survive. The availability of substrates necessary for fetalgrowth may be limited by pathological conditions affecting the placenta, the fetus, and the mother.
- Maternal conditions associated with PFGR interfere with fetal growth by one of the three mechanisms: 1. Causing or aggravating placental vascular insufficiency 2. Limiting the availability of substrates required for fetal growth and development or 3. Transferring to the fetus substances that affect the fetal growth
- The most common causes (75â80% of the cases) of PFGR are abnormalities of the placenta, affecting the maternal or the fetal circulation or both. In the majority of these cases, there is diminished maternal uteroplacental blood flow caused by insufficient or incomplete trophoblastic invasion of the spiral arteries in the placental bed. Under normal conditions, trophoblastic cells first infiltrate the decidua and then the myometrial portion of the spiral arteries, destroying the elastic and muscular layers and replacing them with fibrinoid material. Another feature of abnormal placentation is the deposition of lipoprotein and the infiltration by foamy macrophages of the vascular wall, giving the appearance of accelerated atherosclerosis. The rigid vessel walls are transformed into flaccid sac-like structures that can accommodate the increased uteroplacental blood flow that occurs during pregnancy. These transformed spiral arteries are not affected by maternal vasoregulatory mechanisms. The initial phase of the trophoblastic invasion of the spiral arteries usually ends by the 16th week of gestation, but in many cases completion of the adaptative changes does not occur until 20â22 weeks. When placentation is abnormal, trophoblastic invasion is largely confined to the decidual layer with absent or incomplete changes in the myometrial portion of the spiral and radial arteries. The presence of spiral and radial arteries with intact muscular and elastic layers causes increased vascular resistance and decreased blood flow to the intervillous space, restricting the maternal capacity to provide oxygen and nutrients to the fetus. Also, the vessels with absent or incomplete transformation remain reactive to vasoactive substances produced or ingested by the mother. This placentation defect is not exclusive of FGR and is also found in placentas of women with preeclampsia, preterm labor, and preterm premature rupture of the fetal membranes. Placental infarcts are present in up to 10% of normal pregnancies and they probably result from the hypercoagulability of pregnancy combined with the slow blood flow through the intervillous space. The presence of multiple infarcts is strongly suggestive of the possibility of congenital or acquired maternal thrombophilia. Antiphospholipid antibodies are the most common cause of acquired thrombophilia and factor V Leiden mutation, prothrombin promoter mutation, homozygosity for the methylene-tetra-hydro-folate reductase C677T mutation, and decreased protein S activity are the most common congenitally acquired thrombophilic states. A lesion in the maternal side associated with PFGR is massive perivillous fibrin deposition. In these cases the intervillous space is occupied by fibrin and the villi embedded within the fibrinous mass are nonfunctional. In one study the incidence of PFGR in cases of massive perivillous fibrin deposition was 62.9% (Fuke et al., 1994). This lesion is also present in some cases of fetal demise and is strongly suggestive of the possibility of maternal thrombophilia. Maternal floor infarction is another placental lesion associated with PFGR and fetal demise. Pathologically, this condition is characterized by massive deposition of fibrin in the maternal floor of the placenta encasing the contiguous villi that become necrotic or atrophic. This lesion is apparent macroscopically and can be identified easily by looking at the maternal side of the placenta which will be covered by pale, glassy, smooth tissue with an appearance that vaguely resembles the surface of a brain. Maternal floor infarct is found in 5 per 1000 to 9 per 10,000 births. It is associated with PFGR in more than 50% of cases and is a common finding in cases of fetal death (Mandsager et al., 1994). Unfortunately, this condition frequently reoccurs in successive pregnancies. The pathophysiological basis for maternal floor infarct is unknown but maternal thrombophilia is a good possibility and should be researched systematically. Some investigators consider that maternal floor infarction and massive perivillous fibrin deposition are related conditions (Katzman et al., 2002). Other placental lesions associated with PFGR are chronic villitis, hemorrhagic endovasculitis, and confined placental mosaicism. Lymphocytic and histiocytic infiltration of the villi are the markers of chronic villitis (Althabe and Labarrere, 1985), a nonspecific lesion that may occur in isolation but frequently is associated with vascular lesions in the maternal or fetal side of the placenta. Chronic villitis may be immunological or viral in origin. When cell infiltration by plasma cells occurs, the possibility of infection by cytomegalic virus is high. Chronic villitis occurs in approximately 8% of normal pregnancies but the incidence increases three- to fourfold in cases of PFGR. Pathological fetal growth restriction is present in approximately 30% of patients with chronic villitis. Hemorrhagic endovasculitis is another lesion associated with poor pregnancy outcome and is histologically characterized by the presence of numerous extravascular erythrocytes infiltrating the villi. It is generally believed that hemorrhagic endovasculitis is another histological manifestation of maternal/fetal thrombophilia. Both chronic villitis and hemorrhagic endovasculitis are frequently present in placentas from women with preeclampsia. In cases of confined placental mosaicism, the chromosomal composition of the placenta is not the same as that of the fetus. In these cases the placenta is usually trisomic and the fetus has a normal karyotype but inherits both homologous chromosomes from one of the parents. Most commonly the placenta is trisomic for chromosome 16 but up to 12 other chromosomes could be involved. Most likely the zygote is originally trisomic with subsequent expulsion of one of the trisomic chromosomes from the embryonic but not from the trophoblastic tissue (Robinson et al., 1997). Confined placental mosaicism and fetal uniparental disomy is a condition associated with severe PFGR but may also occur in newborns with normal weight and in some that are large for gestational age. Clotting and thrombosis may also be present in the fetal side of the placental circulation. In these cases the intravascular clotting affects the chorionic stem vessels, causing an infarct with avascular fibrous villi in the distribution territory of the affected vessel. This lesion has been named fetal thrombotic vasculopathy (Redline and Pappin, 1995). In many cases the lesions in the fetal circulation occur simultaneously with infarcts or decidual CHAPTER 4 FETAL GROWTH RESTRICTION 109 vasculopathy in the maternal side of the placenta but in other cases they may occur without apparent maternal side lesions. In any case, the presence of fetal thrombotic vasculopathy has a strong association with poor pregnancy outcome (Arias et al., 1998). Of particular importance is the possibility of an association between this placental lesion and thromboembolic lesions in the fetal brain (Rayne and Kraus, 1993). Placental vascular insufficiency and impaired fetal growth of one or more fetuses are a relatively common finding in multifetal pregnancies. When the restriction in growth affects only one of the fetuses is named âselective FGRâ condition that may occur in up to 21% of multifetal pregnancy. The problem occurs more frequently in twins with monochorionic placentation. Abnormal insertion of the umbilical cord, torsion of the cord, hemangiomas of the placenta, and placenta previa are situations also frequently associated with selective FGR. The overall prevalence of these abnormalities is low.
- The frequency of congenitally abnormal newborns among severely affected PFGR fetuses is approximately 10%. The majority of these genetically affected babies have asymmetric measurements in prenatal ultrasound examination with the head being larger than the abdomen. PFGR is common in chromosomal disorders, especially in somatic trisomies. It also occurs in patients with familial dysautonomy, osteogenesis imperfecta, and other multifactorial disorders. Single gene mutations do not affect fetal growth as much as do chromosomal defects. The possibility of a fetal congenital disorder should always be considered in patients with âidiopathicâ or âunexplainedâ FGR. In a study of more than 13,000 malformed infants born in Atlanta (Khoury et al., 1988) the overall frequency of PFGR was 22.3%. The most common abnormalities associated with PFGR were chromosomal, particularly trisomy 18. The mechanism of fetal growth impairment secondary to genetic syndromes is unknown but it is possible that chromosomal defects cause alterations in placental function, resulting in fetal malnutrition. A large number of fetuses affected by genetic conditions can be detected by a comprehensive or genetic ultrasound examination. Fetal infections are not a common cause of PFGR.Bacterial infections usually have acute courses and cause preterm labor, preterm rupture of membranes, or fetal death. Viral infections on the other hand may be chronic and affect fetal growth. The viral infections associated with impaired fetal growth are congenital rubella, cytomegalic virus, congenital varicella, human immunodeficiency virus, and acute herpes simplex virus infection
- The problems in diagnosing and managing pregnancies with impaired fetal growth are substantial. This is due to the confusion between fetuses that are small and healthy and those who have a pathological restriction in their growth, to our inability to know what is the growth potential of a given fetus, to the occurrence of FGR in patients without recognizable high-risk factors, to the proliferation of measurements to assess fetal growth, to the difficulties in estimating gestational age, and to different opinions about the ideal time to deliver these small fetuses.
- Fig. 2. Fetal deterioration and monitoring in early-severe FGR. Placental disease affects a large proportion of the placenta, and this is reflected in changes in the UA Doppler in a high proportion of cases. The figure depicts in a schematic and simplified fashion the pathophysiologic progression with the main adaptation/consequence in placental-fetal physiology, and the accompanying cascade of changes in Doppler parameters. The sequence illustrates the average temporal relation among changes in parameters, but the actual duration of deterioration is influenced by severity. Regardless of the velocity of progression, in the absence of accompanying PE this sequence is relatively constant, particularly as regards endstage signs and the likelihood of serious injury/death. However, severe PE may distort the natural history and fetal deterioration may occur unexpectedly at any time (see text for abbreviations).
- Fig. 3. Fetal deterioration and monitoring in late-mild FGR. Placental disease is mild and UA Doppler values are not elevated above the 95th centile. The effects of fetal adaptation are best detected by the CPR, which can pick up mild changes in the AU and MCA Doppler. An important fraction of cases do not progress to baseline hypoxia so that they remain only with abnormal CPR. Once baseline hypoxia is established, placental reserve is minimal and progression to fetal deterioration may occur quickly, as suggested by the high risk of severe deterioration or intrauterine fetal death after 37 weeks in these cases, possibly due to a combination of a higher susceptibility to hypoxia of the term-mature fetus and the more common presence of contractions at term (see text for abbreviations).
- Stage I Fetal Growth Restriction (Severe Smallness or Mild Placental Insufficiency). Either UtA, UA or MCA Doppler, or the CPR are abnormal. In the absence of other abnormalities, evidence suggests a low risk of fetal deterioration before term. Labor induction beyond 37 weeks is acceptable, but the risk of intrapartum fetal distress is increased [44]. Cervical induction with Foley catheter is also recommended. Weekly monitoring seems reasonable. Stage II Fetal Growth Restriction (Severe Placental Insufficiency). This stage is defined by UA absent-end diastolic velocity (AEDV) or reverse AoI. Although evidence for UA AEDV is stronger than that for AoI, observational evidence suggests an association between the latter to abnormal neurodevelopment, so that both criteria become a single category. Delivery should be recommended after 34 weeks. The risk of emergent cesarean section at labor induction exceeds 50%, and, therefore, elective cesarean section is a reasonable option. Monitoring twice a week is recommended. Stage III Fetal Growth Restriction (Advanced Fetal Deterioration, Low-Suspicion Signs of Fetal Acidosis). The stage is defined by reverse absent-end diastolic velocity (REDV) or DV PI >95th centile. There is an association with a higher risk of stillbirth and poorer neurological outcome. However, since signs suggesting a very high risk of stillbirth within days are not present yet, it seems reasonable to delay elective delivery to reduce as possible the effects of severe prematurity. We suggest delivery should be recommended by cesarean section after 30 weeks. Monitoring every 24â48 h is recommended. Stage IV Fetal Growth Restriction (High Suspicion of Fetal Acidosis and High Risk of Fetal Death). There are spontaneous FHR decelerations, reduced STV (<3 ms) in the cCTG, or reverse atrial flow in the DV Doppler. Spontaneous FHR deceleration is an ominous sign, normally preceded by the other two signs, and thus it is rarely observed, but if persistent it may justify emergency cesarean section. cCTG and DV are associated with very high risks of stillbirth within the next 3â7 days and disability. Deliver after 26 weeks by cesarean section at a tertiary care center under steroid treatment for lung maturation. Intact survival exceeds 50% only after 26â28 weeks, and before this threshold parents should be counseled by multidisciplinary teams. Monitoring every 12â24 h until delivery is recommended. Particularly at early gestational ages, and at whatever stage, coexistence of severe PE may distort the natural history and strict fetal monitoring is warranted since fetal deterioration may occur unexpectedly at any time.