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Fetal growth restriction; Preterm; Diagnostic parameters; Doppler; Fetal heart rate monitoring

Introduction

Percentile of gestational age, resulting in increased risk of perinatal morbidity and mortality and activation of anaerobic metabolism. , may increase neonatal morbidity/mortality. Perinatal morbidity/mortality in early pregnancy. 32 weeks gestation increased further [1]. Selective FGR administration reduces stillbirth but increases neonatal morbidity and mortality due to iatrogenic preterm birth. Very early her FGR survival is minimal and is usually associated with severe morbidity and neurological sequelae [2]. Monitoring pregnancies with early preterm FGR is challenging, especially with respect to timing of delivery. Finding optimal methods for timely detection of fetal hypoxemia and asphyxia for planning elective birth is essential for many studies. Monitoring is by ultrasound (US) and fetal heart rate (FHRM) monitoring. FHRM is assessed visually for fetal heart rate (FHR), heart rate, variability, acceleration, and deceleration. US monitoring includes biophysical profile values (BPS), amniotic fluid index (AFI), and color Doppler measurements of cord, brain, and venous blood flow. Delivery decisions are relatively straightforward when all methods show consistent results. H. Good or poor fetal condition, especially if maternal findings differ. In early pregnancy, a dilemma may arise as to which diagnostic parameter should be prioritized if conditions are found to be satisfactory [3].

Our study aimed to compare different diagnostic parameters in growth-restricted preterm infants with and without morbidity/ mortality and to monitor preterm pregnancies with early growth restriction 32 weeks to determine the sensitivity and specificity of diagnostic parameters [4].

Materials and Methods

The study examined 120 preterm infants of her who had a gestational age of 32+0 weeks or less and were diagnosed prenatally with placental dysplasia [5]. All pregnancies were of fixed gestational age (until the last menstrual period, confirmed by ultrasonography of the first pregnancy) and were singleton pregnancies without congenital malformations, chromosomal abnormalities, or congenital infections. All patients were divided into her three groups of 40 cases each based on neonatal status. The study aimed to create groups with the same number of patients. Ninety patients were recruited after admission and followed prospectively. After delivery and neonatal follow-up, each patient was assigned to the appropriate group [6]. This group retrospectively included 30 patients who were treated and delivered at the same hospital, selected when their postnatal neonatal outcomes were known. Diagnosis of FGR was made during pregnancy from estimated fetal weight and confirmed when neonatal weight fell below the 10th percentile of the population after delivery. Asymmetric FGR measures Ponderal index (birth weight/crown heel length 3 × 100) using fetal growth parameters (HC/AC, FL/BPD, and FL/AC) during pregnancy and postnatally diagnosed by, was diagnosed by measuring subcutaneous adipose tissue 12 hours postpartum. FGR was diagnosed when these measures fell below the 10th percentile according to the population and Rodriguez tables [7]. Placental FGR was diagnosed by measuring uterine artery blood flow and defined as a mean PI and/or mean RI above the 95th percentile and defined by the presence of a notch [8].

Discussion

An observational clinical study was conducted at the obstetrics and gynecology clinic “Narodny Front” in Belgrade. The study examined 120 preterm infants of her who had a gestational age of 32+0 weeks or less and were diagnosed prenatally with placental dysplasia [9]. All pregnancies were of fixed gestational age (until the last menstrual period, confirmed by ultrasonography of the first pregnancy) and were singleton pregnancies without congenital malformations, chromosomal abnormalities, or congenital infections. All patients were divided into her three groups of 40 cases each based on neonatal status. I - neonates with morbidity/mortality (NMM); II - neonates without acidosis/asphyxia morbidity (NAA); III - neonates without neonatal morbidity/acidosis/asphyxiation (NWMAA). The study aimed to create groups with the same number of patients. Ninety patients were recruited after admission and followed prospectively. After delivery and neonatal follow-up, each patient was assigned to the appropriate group. This group retrospectively included 30 patients who were treated and delivered at the same hospital, selected when their postnatal neonatal outcomes were known. All patients had signed an informed consent form. Diagnosis of FGR was made during pregnancy from estimated fetal weight using Hadlock’s formula and confirmed when neonatal weight fell below the 10th percentile of the population after delivery. Asymmetric FGR measures Ponderal index (birth weight/crown heel length 3 × 100) using fetal growth parameters (HC/AC, FL/BPD, and FL/AC) during pregnancy and postnatally Diagnosed by was diagnosed by measuring subcutaneous adipose tissue 12 hours after delivery. FGR was diagnosed when these measures fell below the 10th percentile, according to the population and Rodriguez tables. Placental FGR was diagnosed by measuring uterine artery blood flow and defined as a mean PI and/or mean RI above the 95th percentile and defined by the presence of a notch [10].

Conclusions

If fetal growth is restricted before 32 weeks, we can conclude that expectant management with intensive fetal monitoring is the best option. Various diagnostic parameters help monitor early fetal growth restriction. In early fetal growth restriction, normal cerebral blood flow is a strong indicator of favorable outcome, and pathologic venous blood flow is associated with poor outcome. Despite established surveillance protocols, individual management remains the best option for optimal delivery timing in fetal growth restriction before 32 weeks.

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2. Bordessoule, Alice (2012) . Pediatric Research72:194–202.

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4. Moorhead, Katherine T (2011) .  IFAC Proceedings 44:569–574.

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5. Carteaux, Guillaume (2012) Chest. 142:367–376.

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6.  Branson R. D (2013). Respiratory Care 58:973–989.

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7. Van Kaam, Anton (2011) . Neonatology 99:338–341.

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8. Howard Stein, Kimberly Firestone, BS, Peter C, Rimensberger (2018) 

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10. Woodward M, Frank D (2002) BJU Int 89: 149-156.

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