Placental insufficiency and fetal growth retardation syndrome

Placental insufficiency (PI) is a clinical syndrome caused by morphofunctional changes in the placenta and disorders of compensatory and adaptive mechanisms that ensure normal growth and development of the fetus, as well as adaptation of the woman's body to pregnancy. Placental insufficiency is the result of a complex reaction of the fetus and placenta to various pathological conditions of the mother's body and is manifested in a complex of disorders of the transport, trophic, endocrine and metabolic functions of the placenta, underlying the pathology of the fetus and newborn. Its clinical manifestations are fetal growth retardation syndrome and/or fetal hypoxia.

Placental insufficiency is a pathophysiological phenomenon consisting of a complex of disorders of the trophic, endocrine and metabolic functions of the placenta, leading to its inability to maintain adequate and sufficient exchange between the mother and fetus. Placental insufficiency syndrome has a multifactorial nature. It has now been established that this pathological phenomenon accompanies almost all pregnancy complications. Habitual miscarriage is complicated by placental insufficiency, according to literature data, in 47.6-77.3% of cases. At the same time, there is an unfavorable background for the onset of pregnancy, caused by hormonal insufficiency, functional and structural inferiority of the endometrium, chronic endometritis, uterine malformations, autoimmune and other disorders of the reproductive system, which often lead to the formation of not only developmental delay in the fetus, but also severe chronic hypoxia.

Fetal growth restriction (FGR), intrauterine fetal growth restriction, small-for-gestational age, and low birth weight are terms used to describe a fetus that has not reached its growth potential due to genetic or environmental factors. The generally accepted cutoff is <10th percentile for gestational age.

Epidemiology

Placental insufficiency is equally often observed in obstetric and extragenital pathology in pregnant women and accounts for 22.4–30.6%. Thus, in case of threatened miscarriage, placental insufficiency is diagnosed in more than 85% of women, in case of gestosis — in 30.3%, in case of arterial hypertension — in 45%, in case of anemia and iso-serological incompatibility of blood of mother and fetus — up to 32.2%, in case of uterine myoma — in 46%, in case of diabetes mellitus — in 55%, in case of lipid metabolism disorders — in 24% of pregnant women. Perinatal mortality in case of placental insufficiency reaches 40%, perinatal morbidity — 738–802‰. At the same time, the share of hypoxic-ischemic damage to the central nervous system accounts for 49.9%, which is 4.8 times higher than in case of uncomplicated pregnancy; respiratory failure and aspiration syndrome are observed in 11% of newborns, and resuscitation measures are required in 15.2%. The incidence of IUGR varies in the population from 10 to 23% of full-term newborns in developed and developing countries, respectively. The frequency of IUGR increases with decreasing gestational age. The presence of congenital malformations, intrauterine hypoxia, transient cardiorespiratory disorders, chromosomal aberrations, intrauterine infections, as well as prematurity significantly (up to 60%) increase the risk of perinatal losses.

Thus, among full-term newborns weighing 1500–2500 g, perinatal mortality is 5–30 times higher, and among children weighing less than 1500 g, it is 70–100 times higher than among newborns with normal gestational weight. Placental insufficiency is a potential cause of premature birth, preeclampsia, IUGR, and stillbirth, which can affect 10–15% of pregnancies. [ 1 ], [ 2 ]

70% of fetuses and newborns whose body weight is not higher than the 10th percentile for the gestational age are small due to constitutional factors (female gender, mother's belonging to certain ethnic groups, parity of births, weight and height characteristics of the mother), however, among these children, perinatal mortality rates do not differ from those in children with normal body weight for the gestational age.

Moderate and severe fetal growth restriction are defined by body weight from 3 to 10 percentiles and < 3 percentiles, respectively.

Forms

There is no generally accepted classification of placental insufficiency due to its multifactorial etiology. Depending on the structural units in which pathological processes occur, three forms of placental insufficiency are distinguished:

1. hemodynamic, manifested in the uteroplacental and fetal-placental basins;
2. placental-membrane, characterized by a decrease in the ability of the placental membrane to transport metabolites;
3. cellular-parenchymatous, associated with impaired cellular activity of the trophoblast and placenta.

There is also primary fetoplacental insufficiency, which occurs before 16 weeks of pregnancy, and secondary fetoplacental insufficiency, which develops at a later stage.

• Primary placental insufficiency occurs during implantation, early embryogenesis and placentation under the influence of various factors (genetic, endocrine, infectious, etc.) affecting the parents' gametes, zygote, blastocyst, developing placenta and the female reproductive system as a whole. Characteristic are anatomical changes in the structure, location and attachment of the placenta, as well as vascularization defects and chorion maturation disorders. In addition, with this form of fetoplacental insufficiency, fetal malformations, chromosomal abnormalities and intrauterine infection are detected more often than in the population.
• Secondary fetoplacental insufficiency develops under the influence of exogenous factors and is observed in the second half of pregnancy.

Fetoplacental insufficiency (primary and secondary) has an acute or chronic course.

• Acute placental insufficiency occurs as a result of extensive placental infarctions and premature detachment of a normally located placenta with the formation of a retroplacental hematoma, which may result in fetal death.
• Chronic placental insufficiency is observed in every third pregnant woman in the high-risk group for perinatal pathology. It develops early and lasts for a long time, due to the disruption of compensatory-adaptive mechanisms in combination with circulatory disorders, involutional-dystrophic changes and inflammation/exacerbation associated with the woman's illness during pregnancy.

At present, it is more appropriate to distinguish decompensated, subcompensated and compensated forms. This classification is based on the degree of fetal growth retardation, the presence and severity of signs of chronic intrauterine fetal hypoxia, the degree of hemodynamic disturbances in the mother-placenta-fetus system, the severity of placental hormonal function disorders, and the effectiveness of the treatment.

The process of fetal growth consists of three successive phases.

• The first phase - the phase of cellular hyperplasia - occupies the first 16 weeks of pregnancy.
• The second phase is the phase of simultaneous hyperplasia and hypertrophy, which is a simultaneous increase in the number of cells and an increase in their size, and occupies a period of time between 16 and 32 weeks.
• The third phase is cellular hypertrophy, which lasts from 32 weeks until delivery and is characterized by a rapid increase in cell size. When quantitatively assessing the rate of fetal growth, it was found that an increase in fetal weight in a singleton pregnancy by 5 g/day is noted at 14–15 weeks, 10 g/day at 20 weeks, and 30–35 g/day at 32–34 weeks. Subsequently, the rate of weight gain decreases.

Classification of fetal growth retardation syndrome is possible only when performing extended ultrasound fetometry during dynamic examination of the pregnant woman. According to the form, the following are distinguished: symmetrical - with an even lag in all fetometric indicators (20-30% of all observations); asymmetrical - a predominant decrease in the size of the fetal abdomen (70-80%) and mixed - a decrease in all fetometric indicators with a predominant decrease in the size (girth) of the fetal abdomen (5-10%).

According to the severity in the antenatal period, the following are distinguished:

• Grade I - fetometric parameters are 1–2 weeks behind those expected for the gestational age;
• II degree - delay of 2-4 weeks;
• Grade III - delay of more than 4 weeks.

Diagnostics Placental insufficiency and fetal growth retardation syndrome

To diagnose fetal growth restriction (FGR), it is important to accurately estimate the gestational age. Although this value is usually calculated based on the last menstrual period, if known with certainty, the reliability of this estimate is low because the timing of ovulation varies. A first trimester ultrasound can date the pregnancy more accurately.

In both developed and developing countries and across all racial and ethnic groups, there is a positive association between total maternal weight gain and fetal birth weight. Inadequate early pregnancy weight gain (less than 4.3 kg) before 24 weeks is an independent predictor of low birth weight.

Serial assessment of the bottom height of the bottom

Serial fundal height measurement is a simple method for assessing fetal growth. Measurements are taken from the fundus to the pubic symphysis using a non-elastic tape with the centimeter side down.

Biochemical markers

Coyle and Brown in 1963 reported significantly lower urinary estriol levels in pregnancies with small infants. The development of radioimmunoassays facilitated the shift from urinary estriol to blood estriol. Unfortunately, significant diurnal variability in urinary excretion rates and diurnal variations in plasma concentrations made interpretation difficult. Human placental lactogen (hPL) was first proposed in the late 1960s as a marker of placental function. Studies of normal and abnormal pregnancies led to the concept of the fetal danger zone, in which plasma hPL concentrations below 4 μg/mL after 30 weeks of gestation are classified as abnormally low and indicate a high-risk pregnancy. However, because a significant number of fetal deaths could occur in association with normal hPL concentrations, this assay was not widely used [2].

Ultrasonographic biometry

Ultrasound measurements of biparietal diameter, head circumference, abdominal circumference, and femur length are recorded and compared with the 50th percentile of the corresponding parameter in the prepared population charts. Measurements below the 10th percentile are highly suspicious of IGR, and measurements below the 3rd percentile are unequivocal evidence of IGR. An increase in abdominal circumference of less than 1 cm in 14 days also indicates IGR.

Ponderal index

The estimated fetal weight [3] is less than the 10th percentile. Based on the Ponderal index, two types of hPL are described:

Symmetrical FGR. These infants have a normal Ponderal index, in which weight and length are limited in growth, and infants have a small head circumference. Early growth restriction is suggested.

Asymmetrical FGR. These children have a low Ponderal index, where weight is limited more than length. Here, there is a late onset of growth restriction.

Amniotic fluid is isolated from fetal urine and the respiratory tract. In IUGR, shunting of blood from the splanchnic circulation results in decreased renal blood flow, decreased glomerular filtration rate, and hence decreased fluid volume. The amniotic fluid index is measured by adding the vertical depth of the non-cord pockets of amniotic fluid in each of the four quadrants of the uterus. A total depth of 5 cm or more is normal. Similarly, a single vertical pocket of amniotic fluid measuring more than 2 cm is normal.

Another sign of IGR is the presence of placental calcium deposits, which indicates placental aging. Detection of grade 3 placenta before 36 weeks is confirmatory evidence of IGR [3].

The role of Doppler. Doppler of the uterine arteries

The uterine arteries provide the majority of the blood supply to the uterus. During pregnancy, uterine blood flow increases 10- to 12-fold due to trophoblastic invasion of the myometrial and decidual spiral arteries and a 50% increase in maternal blood volume. The uterine artery Doppler waveform is unique and changes as pregnancy progresses. Early in pregnancy, the uterine circulation is characterized by high resistance and low flow, yielding a waveform with constant end-diastolic velocity and continuous forward blood flow throughout diastole. As trophoblastic invasion and spiral artery modification continue, placental perfusion increases and the uteroplacental circulation becomes a high-flow, low-resistance system, yielding a waveform with high end-diastolic flow.

When normal trophoblastic invasion and modification of the spiral arteries are interrupted, resistance to blood flow in the uterine arteries increases and placental perfusion decreases. These pathological processes are key features common to the development of preeclampsia and IUGR.

A prospective study by Zimmermann et al. [ 3 ] assessed the usefulness of uterine artery Doppler ultrasonography performed between 21 and 24 weeks in predicting the subsequent development of preeclampsia and IUGR. They identified 175 women at high risk of developing hypertensive disorders of pregnancy or IUGR and 172 pregnancies at low risk. Persistent notching or increased RI in the uterine arteries or increased RI in the uteroplacental arteries were defined as abnormal Doppler features. [ 4 ]

Based on currently available data, there is insufficient evidence to recommend uterine artery Doppler ultrasonography as a general screening method for all pregnancies. When performed in a high-risk group, it has some value in identifying pregnancies that may require more frequent blood pressure assessment.

The umbilical artery (UA) was the first vessel to be studied by Doppler. By about 15 weeks of gestation, diastolic flow can be detected in the UA. With increasing gestational age, end-diastolic velocity increases due to a decrease in placental resistance. This is reflected by a decrease in S/D or PI. As the chorionic vascular bed undergoes an atherosclerotic-like process, this leads to local ischemia and necrosis. The umbilical artery exhibits increasing impedance, which initially blunts forward flow during diastole and eventually reverses it later. These findings have been associated with adverse perinatal outcomes. When altered diastolic flow is detected, steroids should be considered for preterm lung maturity and delivery.

The middle cerebral artery (MCA) is another vessel well characterized by Doppler ultrasound that has also been shown to be affected by IUGR. The MCA typically exhibits low amplitude diastolic flow that increases in the presence of fetal hypoxia as a marker of cerebral vasodilation. This most often represents a later stage of the hypoxic process and usually occurs after changes in the uterine artery.[ 5 ]

Dhand et al. [5] compared MCA Doppler indices with umbilical artery Doppler indices in a prospective study of 121 women, of whom 71 were high-risk women with IUGR and 50 women had healthy fetuses. The predictive value of PI Doppler for detecting abnormal fetal outcome was 94% in MCA compared to 83% for umbilical artery. The sensitivity was 71% for MCA compared to 44% for umbilical artery. Thus, the authors concluded that MCA Doppler indices are a better predictor of fetal outcome in IUGR compared to umbilical artery in terms of sensitivity and predictive value.

The sequence of abnormal events that portends adverse perinatal outcome begins with absent MV end-diastolic flow. Later findings include abnormal MCA Doppler pulsatility (with decreased IP) and abnormal ductus venosus flow (absent or reversed flow during atrial contraction) and reversed flow in the AF. These changes are significantly associated with perinatal mortality.

Management of fetuses with abnormal Doppler values depends on the gestational age. In mature fetuses, continued pregnancy is of little benefit and the time to decompensation is usually shorter in these fetuses, so delivery is recommended. Induction of labor may be appropriate in those with reliable fetal heart monitoring. Careful monitoring is necessary in immature fetuses.

If no end-diastolic flow is detected in the AF, biophysical profile (BDP) and Doppler indices should be measured twice a week, and daily fetal kick counts are recommended. In the presence of AF flow reversal or MCA cephalization, hospitalization with continuous oxygen therapy, bed rest, daily BDP, and daily Doppler examination is indicated. Steroids should be administered to achieve fetal lung maturity. [ 6 ]

A pulsatile DW pattern indicates fetal acidemia and is an indication for delivery. A fetus with reversed end-diastolic flow in the AF and/or a pulsatile DW pattern has little reserve and will likely not survive delivery.

3-D power Doppler is particularly sensitive for detecting low-velocity flow, which is then visualized to provide detailed images of small vascular structures. Because tertiary trunk villi can be visualized, there is the potential for earlier detection of abnormal placentas to identify pregnancies at high risk for preeclampsia or IUGR or to evaluate suspected placental abruption or accreta [6].

Placental MRI in intrauterine growth retardation

Fetal MRI is now recognized as an adjunct to ultrasound in the diagnosis of fetal anomalies. Damodaran et al. [ 7 ] studied placental MRI in singleton fetuses with growth restriction. The authors found that fetuses with growth restriction had a significant increase in the volume of placenta affected by pathology. The placenta also became thickened and globular, with an increase in the placental thickness to volume ratio. Although placental volume increased with increasing gestational age, it remained reduced in fetuses with growth restriction. The authors concluded that placental MRI imaging is indicative of the severity of the underlying disease in fetal growth restriction.

Read also: Placental Insufficiency - Diagnosis

Treatment Placental insufficiency and fetal growth retardation syndrome

Bed rest in hospital or at home is widely recommended. This allows for close monitoring. However, the benefits of bed rest must be balanced against the risk of thrombosis. Gulmezoglu and Hofmeyr evaluated the role of bed rest in fetal growth restriction. The authors compared bed rest with outpatient treatment in women with fetal growth restriction. There were differences in fetal weight and birth weight in both groups, but the difference was not statistically significant. [ 8 ]

Nutritional Supplements for Mother

Maternal dietary supplementation through balanced calorie intake, rather than specific protein supplements, has variable effects on fetal growth. The effect is small, although fetal weight has been shown to increase by 100–300 g. Ramakrishnan et al. [ 9 ] conducted a randomized, double-blind, placebo-controlled trial of the effects of docosahexaenoic acid supplementation during pregnancy on gestational age and birth size.

Nitric oxide donors

L-Arginine improves uteroplacental blood flow by overcoming placental ischemia by increasing nitric oxide. This results in uterine vasodilation. Neri et al. [ 10 ] evaluated the effect of infusion of l-arginine (ARG), a nitric oxide substrate, on uteroplacental blood flow in the third trimester. Three groups of nine women each were infused with 30 g of ARG over 30 minutes. One group served as a control. The remaining two groups had IUGR, one with increased uteroplacental circulatory resistance and one without increased resistance. The authors found no hemodynamic changes in the uteroplacental circulation. They found that serum nitrite/nitrate as well as serum growth hormone levels were significantly increased by ARG. The authors also reported a significant decrease in resistance in women whose IUGR was due to increased resistance. They concluded that ARG infusion affects the uteroplacental circulation in women with IUGR due to increased resistance. This effect is specific and appears to be mediated by nitric oxide release. Rytlewski et al. [ 11 ] studied the effect of low-dose oral ARG on the biophysical profile, fetoplacental circulation, and neonatal outcome in preeclampsia. This was a randomized, placebo-controlled, double-blind clinical trial. Oral therapy with 3 g ARG daily or placebo was administered as an adjunct to standard therapy. The results showed that l-arginine treatment accelerated fetal weight gain and improved the biophysical profile. Starting from the 3rd week of therapy, the umbilical artery pulsatility values were significantly lower in the ARG group. Infants in this group showed higher Apgar scores. The authors concluded that adjunctive treatment with oral ARG appears promising for improving fetal and neonatal outcomes and for prolonging pregnancies complicated by preeclampsia.

Low dose aspirin

The use of low-dose aspirin for the prevention and treatment of preeclampsia and intrauterine growth restriction has been studied extensively. Leitich et al. [ 12 ] conducted a meta-analysis of low-dose aspirin for the prevention of IUGR. Aspirin use showed a significant reduction in IUGR and a nonsignificant reduction in perinatal mortality. Subgroup analysis showed that aspirin was effective at lower doses of 50 to 80 mg/day, but the preventive effect was greater at higher doses of 100 to 150 mg/day and among women entering the study before 17 weeks of gestation. The authors concluded that low-dose aspirin should not be routinely prescribed to pregnant women.

Indications for the use of low-dose aspirin may include pre-existing chronic hypertension, recurrent preeclampsia, and hypertension before 20 weeks and associated autoimmune diseases such as systemic lupus erythematosus, a positive test for anticardiolipin antibodies, and the presence of lupus anticoagulant. The multicenter FLASP (FOGSI Low-Dose Aspirin Study) trial was conducted by FOGSI to evaluate the effectiveness of low-dose aspirin for the prevention and treatment of preeclampsia and IUGR. The incidence of IUGR and preeclampsia was significantly reduced in patients who received low-dose aspirin prophylactically before 16 weeks of gestation. One of the largest collaborative trials was CLASP - Collaborative Trials of Low-Dose Aspirin in Pregnancy. This trial recommended the use of low-dose aspirin in women particularly prone to early development of preeclampsia severe enough to require preterm delivery.

Heparin

Heparin prevents pregnancy loss by inhibiting complement activation in the trophoblast in addition to its anticoagulant effect. Unfractionated heparin or low molecular weight heparin can be used. The main concern with heparin therapy in pregnancy is osteoporosis, as its use in pregnancy is long-term and pregnancy and lactation also cause reversible bone demineralization. Adequate calcium and vitamin D3 intake and moderate exercise are necessary to prevent spinal collapse. Bone density improves after heparin is discontinued.

Low molecular weight heparins (LMWH) have fewer complications than regular heparin and are more commonly used safely in pregnancy. LMWH inhibits factor Xa and has an antithrombotic effect, while heparin also has an anticoagulant effect through its effect on antithrombin III and factor IIa. Thus, bleeding is rare with small changes in PT and APTT. It can be given once daily and reduces the risk of thrombocytopenia and osteoporosis. Both heparin and LMWH do not cross the placenta and no fetal complications have been reported. Enoxaparin 40 mg/day subcutaneously or Dalteparin 5000 U/day are administered from the time pregnancy is confirmed until delivery.

Sildenafil citrate

Sildenafil citrate, a specific phosphodiesterase inhibitor, is increasingly used for pulmonary hypertension during pregnancy. Sildenafil is also emerging as a potential candidate for the treatment of intrauterine growth restriction and preterm labor. Maharaj et al. [ 13 ] studied the effects and mechanisms of action of sildenafil citrate in human chorionic arteries ex vivo.

A series of pharmacological studies determined the effect of sildenafil citrate on pre-constricted chorionic plate arterial rings. Their results showed that phosphodiesterase-5 mRNA and protein were detected in human chorionic plate arteries. Sildenafil induced dose-dependent vasodilation. The authors concluded that sildenafil citrate vasodilates feto-placental blood flow through a cGMP-dependent mechanism involving increased sensitivity to nitrous oxide. Von Dadelsen et al. [ 14 ] studied the role of sildenafil citrate therapy in severe early-onset intrauterine growth restriction. Women were offered sildenafil citrate 25 mg three times daily until delivery if their pregnancy was complicated by early-onset IUGR (AC <5th centile) and gestational age was <25 weeks or fetal weight <600 g. The authors found that sildenafil growth was associated with increased AC growth (odds ratio 12.9). Data from randomized controlled trials are needed to determine whether sildenafil improves perinatal outcomes in patients with early-onset IUGR.

Growth Monitoring - Fetal Growth Retardation

Counting fetal movements

Decreased fetal movements are a cause for concern and anxiety. Fetal movements follow a circadian rhythm and are an expression of fetal well-being [15]. Decreased fetal movements are considered a marker of suboptimal intrauterine conditions. The fetus responds to chronic hypoxia by conserving energy, and the subsequent decrease in fetal movements is an adaptive mechanism for reducing oxygen consumption.

Fetal heart rate monitoring

Fetal heart rate monitoring will show a pattern of changes that correlate with fetal deterioration. The usual pattern is no accelerations, decreased variability, and spontaneous decelerations. These changes depend on the severity of the fetal lesion and the gestational age of the fetus. It is unusual to have an acceleration pattern at less than 32 weeks, even if the fetus is not at risk.

HR monitoring is a sensitive indicator of fetal hypoxia and acidosis, but it lacks specificity and has a significant number of false-positive results.

Biophysical profile

The biophysical profile is a combination of ultrasound monitoring of fetal behavior (fetal breathing, fetal movements, fetal tone, and amniotic fluid volume) and heart rate monitoring and is a sensitive test for detecting depletion of fetal reserves.

Delivery of a fetus with growth retardation

The optimal management strategy is to avoid delivery of a premature infant who adequately compensates for placental dysfunction and to recommend delivery when initial signs of acidemia are detected. The following changes suggest the onset of fetal acidemia.

• Fetal heart rate monitoring: no accelerations, no or minimal variability
• Dopplerography of the umbilical artery: no diastolic blood flow.
• Biophysical Profile 6
• Ductus venosus: decreased or absent direct blood flow during atrial contraction.

The full-term fetus has a high capacity to tolerate the hypoxic stress of labor. This capacity is significantly reduced in fetal growth restriction due to severe depletion of energy stores in the liver and subcutaneous tissues. In hypoxia, energy stores are rapidly depleted, and the fetus must switch to anaerobic metabolism to produce energy. Unfortunately, anaerobic metabolism produces large amounts of hydrogen ions, and metabolic acidosis occurs. Thus, intrapartum asphyxia is a major cause of perinatal morbidity and mortality in fetal growth restriction. Therefore, when umbilical Doppler sonography shows absent or reversed diastolic flow, cesarean section is indicated. In patients with increased umbilical artery resistance, vaginal delivery can be attempted under close observation, but in many of these patients, cesarean section should be expected.

During labor, the fetal heart rate should be closely monitored, and changes in fetal heart rate that suggest fetal dysfunction should be followed by cesarean section. The second stage of labor requires special attention. In most cases, it is preferable to avoid pushing during the second stage and allow the fetus to descend solely under the influence of uterine contractions. It is not recommended to prolong the second stage beyond 2 hours in nulliparous women and 1 hour in multiparous women.[16]

Intranatal monitoring

Auscultation of the fetal heart rate

Intranatal monitoring is mainly aimed at detecting fetal asphyxia in order to prevent perinatal mortality or future neurodevelopmental disorders. Bradycardia, tachycardia, and irregular pulse are signs of asphyxia.

Electronic fetal monitoring

Labor contractions reduce uteroplacental blood flow and/or compress the umbilical cord depending on its position and the amount of amniotic fluid. Reduced blood flow may endanger fetuses that have already experienced hypoxia. Signs of decreased variability of baseline parameters, decelerations, and lack of accelerations suggest fetal hypoxia.

Fetal pulse oximetry

Fetal pulse oximetry appears to be a promising new tool for intrapartum fetal monitoring. It is not only accurate and rapid in measuring fetal oxygenation, but also allows direct assessment (rather than indirect assessment as with heart rate monitoring) of fetal oxygenation and peripheral tissue perfusion. Fetal pulse oximeters measure the fraction of light that is not absorbed after passing through the pulsatile vascular bed. The sensors are placed on the skin surface, such as the head or face of the fetus. Sensor placement is straightforward when the cervix is more than 2 cm dilated.[17]

Scalp blood pH

In 1962, Saling introduced fetal scalp blood sampling during labour. It is a useful aid in detecting fetal acidosis when there is difficulty in interpreting abnormal CTG traces. With accumulation of CO2 due to decreased placental gas exchange, pH decreases due to respiratory acidosis. Increased hypoxia leads to anaerobic metabolism resulting in production of lactate and hydrogen ions (H+). Low pH has been used as one of the best available parameters to detect intrapartum asphyxia. Although this method has been used effectively in many centres abroad, very few have used this method in India.

Read also: Placental insufficiency - Treatment

Prevention

• treatment of extragenital diseases before pregnancy;
• correction of metabolic disorders and blood pressure from the early stages of gestation;
• maintaining a rational diet and daily routine for the pregnant woman;
• according to indications, prescribe antiplatelet agents (acetylsalicylic acid at a dose of 100 mg/day, dipyridamole at 75 mg/day and pentoxifylline at 300 mg/day) and anticoagulants (nadroparin calcium, dalteparin sodium);
• according to indications, use of deproteinized hemoderivative from the blood of dairy calves (Actovegin) 200 mg 3 times a day for 21–30 days;
• the use of gestagens (dydrogesterone, microionized progesterone) in pregnant women with habitual pregnancy loss from early gestation;
• prescribing multivitamin complexes.

Forecast

Timely diagnosis of placental insufficiency and IUGR, correct and competent management of pregnant women allow prolonging pregnancy until the term of birth of a viable fetus with a favorable perinatal outcome. The choice of the term of delivery should be based on a set of diagnostic tests. In case of early delivery, it is necessary to take into account the availability of conditions for intensive care and resuscitation of newborns.

Children with low birth weight have a high risk of physical, neuropsychic developmental disorders and increased somatic morbidity. The most common symptoms observed in newborns are:

• disorders of cardiopulmonary adaptation with perinatal asphyxia, meconium aspiration or persistent pulmonary hypertension;
• in the case of a combination of IUGR and prematurity - a high risk of neonatal death, necrotizing enterocolitis, respiratory distress syndrome, intraventricular hemorrhage;
• disturbances in thermoregulation due to increased heat loss (due to a decrease in the subcutaneous fat layer) or decreased heat production (depletion of catecholamines and reduced delivery of nutrients);
• hypoglycemia (in 19.1% of newborns);
• polycythemia and hypercoagulation (diagnosed in 9.5% of cases of stage I IUGR and in 41.5% of cases of stage III);
• reduced immunoreactivity (neutropenia is detected in 50% of newborns with stage III IUGR, and nosocomial infections in 55%).

Physical development disorders

Newborns with low birth weight have different variants of physical development, depending on the etiology and severity of intrauterine growth retardation. In case of moderate IUGR, high growth rates are observed during 6–12 months after birth, during which children achieve normal weight-height ratios. However, according to some data, newborns achieve normal body weight within 6 months after birth, but retain a growth deficit of 0.75 standard deviations during the first 47 months of life compared to children with normal birth weight. In case of severe IUGR, weight and height lag below the 10th percentile persist not only in childhood but also in adolescence. Thus, the average height at the age of 17 with severe intrauterine growth retardation is 169 cm for boys and 159 cm for girls versus 175 cm and 163 cm with normal birth weight, respectively.

Neuropsychic developmental disorders

Many researchers note a decrease in IQ and significant learning difficulties in severe IUGR (birth weight less than 3rd percentile), especially in premature pregnancy. Thus, at the age of up to 5 years, children have minor brain dysfunctions, motor disorders, cerebral palsy and poor cognitive abilities 2.4 times more often than with normal birth weight; 16% of children aged 9 years need remedial education; 32% of adolescents with severe IUGR have significant learning problems that prevent them from completing a full course of secondary school. In a study conducted by LM McCowan (2002), 44% of newborns with IUGR caused by hypertension of pregnancy have a low mental development index. Disorders of psychomotor development are more often noted in newborns who were not breastfed for at least the first 3 months of life, who were hospitalized for a long time, and who required artificial ventilation.

Adults born with low birth weight have a higher risk of coronary heart disease, arterial hypertension, cerebrovascular accidents, diabetes, and hypercholesterolemia. Thus, among men, mortality from cardiovascular diseases was 119‰ with a birth weight of 2495 g versus 74‰ with a birth weight of 3856 g. Animal studies have shown that disruption of the trophic function of the placenta leads to structural and functional adaptation that ensures the survival of the newborn. Subsequently, the adaptation stress experienced leads to the development of the above diseases.

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