Identification of Fetal Intrauterine Growth Restriction in Pregnancy-Induced Hypertension Women in Saudi Arabia

The second most frequent medical condition found during pregnancy is hypertension, which, combined with bleeding and infection, significantly increases maternal complications and death.¹ Pregnancy-induced hypertension (PIH), a significant cause of maternal and neonatal morbidity and mortality, has virtually disappeared from the clinical landscape in developed countries thanks to better prenatal care and rapid medication.² However, it remains a significant obstetric issue in developing nations like ours and among the rural populace, and its consequences are to blame for the majority of PIH mortality.³ Pregnancy-related hypertension has an impact on the outcome of the foetus and is linked to intrauterine death, low birth weight, and a higher risk of admission to the neonatal intensive care unit. It was discovered to be the main reason for stillbirth in a hospital-based study from MCH Sakaka, Aljouf, Saudi Arabia. While the cause of hypertensive disorders of pregnancy is yet unknown, the rate of virulence from hypertension during pregnancy is significantly more in underdeveloped countries than in the developed world.⁴ It is frequently believed that PIH and unexplained intrauterine growth restriction are connected to placental insufficiency and intimately linked to placental malfunction, which causes foetal growth restriction. Foetuses with birth weights below the 10th percentile for gestational age are said to have intrauterine growth restriction (IUGR).⁵ Intrauterine growth restriction is thought to affect 5% of pregnant women in general, and it affects 28% of pregnant women in PIH. Low Apgar scores (19%), abortion (11%), low birth weight (31%), preterm birth (2%), stillbirth (10%), neonatal morbidities and deaths, and even long-term effects on children are all caused by IUGR.⁶ Reducing prenatal and neonatal problems, mortality, and morbidity is facilitated by early identification of intra-uterine growth limitations.⁵ Hence, the aim of our study is to the assessment of the IUGR in pregnancy-induced hypertension women.

MATERIAL AND METHODS

The Maternity and Children Hospital (MCH) Sakaka, Aljouf, Saudi Arabia, received 162 pregnant women between January 2021 and January 2022 for this cross-sectional study. all pregnant women between the ages of 16 and 45, whether nulliparous or multiparous and were recruited for the study after receiving verbal consent. All of the PIH patients underwent IUGR and outcome evaluations in accordance with the operational definition's criteria (PIH= after 20 weeks of pregnancy, blood pressure greater than 140/90 measured twice, more than six hours apart, without any evidence of protein in the urine, IUGR is defined as a weight below the 10^th percentile for gestational age as seen on ultrasonography. and Apgar score was below 6 at 5 minutes, Babies who were born with low birth weights typically weighed less than 2,500 grams, preterm birth: the delivery of a child before 37 weeks of pregnancy, and Stillbirth: the delivery of a dead child after 24 weeks of pregnancy). By means of clinical examinations and ultrasound, we evaluated each individual. The data was gathered using a pre-made proforma. Considering that there are 162 individuals with pregnancy-induced hypertension, the lowest prevalence of IUGR in PIH is 28%12 d=7%. Women who were expecting were not included, as were those who had ischemic heart disease, connective tissue/autoimmune illnesses, or known chronic renal disease. SPSS version 22.00 was used to analyze the data. The frequency and percentage were calculated taking into account the following factors: IUGR, PIH findings, parity, length of illness, mode of delivery, and maternal and gestational age. Maternal and gestational age, as well as the length of the disease, were determined using the mean and standard deviation (SD). The following characteristics were stratified: maternal and gestational age, mode of birth (cesarean section or vaginal delivery), parity, and length of the disease in order to see their effects on the outcome and manage effect modifiers. Categorical variables were subjected to the post-stratification chi-square test at a 95% confidence level, and a p-value of 0.05 was deemed statistically significant. The University of Jouf's ethical review board gave the study its approval.

RESULTS

Over the course of the 1-year trial period, 162 cases of PIH were assessed for intrauterine growth restriction. Table 1 and Figure 1 show the demographics and clinical characteristics of the study. A total of 105 (64.8%) IUGRs were detected in PIH women.

Figure 1

Normal foetal and IUGR in PIH women

The mean SD values for the total participant group were.84±7.86, 43.61±5.76, 4.83±1.44, 3.00±3.0, 1812±3.33and 4.34±1.30, for the mother's age (years), gestational age (weeks), disease duration (weeks), baby weight (grams), and APGAR score respectively (Table 2).

The outcome was a low Apgar score of 29 (19.3%), abortion of 12 (11.4%), low birth weight of 29 (19.3%), preterm birth of 21 (20%), and stillbirth of 14 (13.3%) in 105 (64.8%) foetal IUGR, as shown in Table 3, Figure 2 and Figure 3.^7,8

Figure 2

Status of IUGR in PIH women

However, our findings and stratification for the factors under research are as follows: Regarding the IUGR in connection to maternal age, the percentages were 37.5% (16–19 years), 25.7% (20–29 years), 28.5% (30–39 years), and 10.4% (40–45 years) [p = 0,00]. The IUGR was 36.1% (21-34 years) and 63.8% (35–42 years) in relation to gestational age [p = 0.05]. The IUGR was 61.9% for nulliparous parity and 38% for multiparous (p=0.00), whereas the IUGR was 53% for cesarean section deliveries and 39.5% for vaginal deliveries (p=0.21). Table 4 shows the relationship between maternal age, gestational age, and parity with stillbirth.

DISCUSSION

When compared to gestations without hypertension problems, hypertensive pregnancies have higher rates of perinatal morbidity and mortality, and the major foetal consequence of these pregnancies is IUGR.⁹ Early morbidity is adversely affected by the degree of intrauterine growth restriction.¹⁰ Through placental microcirculation, the foetus receives nutrients and oxygen from the mother during embryogenesis and development. Pre-eclampsia and pregnancy-induced hypertension are intimately linked to placental malfunction.⁹ The lack of blood that is well-oxygenated and rich in all nutritional components reaching the foetomaternal unit during pregnancy is the direct cause of pregnancy-induced hypertension and intrauterine growth limitation.¹¹ There was a correlation between the mother's parity and pregnancy-induced hypertension. PIH is prevalent in primigravida and is likely the primary cause of IUGR and low placental weight.¹² In our study, 64.8% of patients with IUGR the primigravida (61.9%), and the remaining were multiparous (38%), this is comparable with a study conducted formerly where primigravida was 57.5%, and similar results were reported in a different study.¹³ Our findings are analogous to those of research on IUGR conducted in Japan, where 57% of cases had early-onset PIH and 43% had late-onset PIH.¹⁴ It was discovered such early-onset moderate to severe PIH could raise the danger of foetal death, whereas delivery by cesarean section could lower hazards in PIH-affected women. In line with the earlier study, the current study found that 13.3% and 19.3% of pregnant women with pregnancy-induced hypertension, respectively, had stillbirths.¹⁵ The current study's findings highlighted low birth weight and prematurity as the perinatal repercussions and revealed a low stillbirth rate. Early detection of hypertension and the implementation of the appropriate treatment increased the likelihood of a healthy pregnancy for both the mother and the foetus.¹⁶ The previous study found that pregnancy-induced hypertension was present in 5% of the women who experienced stillbirth, a low birth weight of 16%, and Apgar score of 20%, in addition to preterm birth.¹⁷ The current study's findings revealed a link between PIH and having a child with a w birth weight. The increased risks associated with PIH are concerning because low birth weight is a key predictor of adult health outcomes and also has a long-term impact. Therefore, one of the methods to lower the risk of low birth weight and its effects is to prevent and/or manage PIH.¹⁸ An increased risk of poor perinatal outcomes was linked to hypertensive problems during pregnancy. However, Preterm delivery, low birth weight babies, neonatal death, and low Apgar scores were all more likely to occur in pregnant women with hypertensive diseases. The observation that effective quality improvement programs can contribute to high-quality care in a situation with limited resources highlights the need to maintain the focus on improving care quality.

CONCLUSION

In the current study, intrauterine growth restriction, which is usually a complication of hypertensive disorders of pregnancy, was recorded at 64.8%, with low Apgar scores of 29 (19.3%), abortion at 12, low birth weight at 29, preterm birth at 21, and stillbirth at 14.3% as outcomes. Therefore, in contemporary obstetrics, assessing this growth abnormality is a simple process that may be quickly detected and tracked using clinical and ultrasonographic screening.

REFERENCES

1. Katt AH, Garovic VD. The management of hypertension in pregnancy. Adv Chronic Kidney Dis 2013;20:(3)229–39.
2. Lo JO, Mission JF, Caughey AB. Hypertensive disease of pregnancy and maternal mortality. Curr Opin Obstet Gynecol 2013;25:(2)124–32.
3. Patel R, Baria H, Patel HR, et al. A study on pregnancy-induced hypertension and foetal outcome among patient with PIH at tertiary care hospital, Valsad. Int J Community Med Public Health 2017;4:(11)4277–81.
4. Singh S, Ahmed EB, Egondu SC, et al. Hypertensive disorders in pregnancy among pregnant women in a Nigerian teaching hospital. Niger Med J 2014;55:(5)38.
5. Sharma P, Gyawali M, Gurung SD. Role of umbilical artery Doppler in predicting intrauterine growth restriction and foetal outcome in pregnant ladies with pregnancy-induced hypertension. Nepal J Radiol 2017;7:(10)3–8.
6. Maged M, Wageh A, Shams M, et al. Use of sildenafil citrate in cases of intrauterine growth restriction (IUGR); a prospective trial. Taiwan J Obstet Gynecol 2018;57:483–6.
7. Dawood Y, Buijtendijk M, et al. Imaging fetal anatomy. Semin Cell Dev Biol 2022;131:78–92.
8. Wu W, Ji Q, Guo B, et al. Clinical value of serum homocysteine, folate, and ultrasonography detection of yolk sac in predicting the outcome of threatened abortion. Pteridines 2019;30:10–15.
9. . Gortner L. Intrauterine growth restriction and risk for arterial hypertension: a causal relationship? J Perinat Med. 2007;35:(5)361-5.
10. Sehested LT, Pedersen P. Prognosis and risk factors for intrauterine growth retardation. Dan Med J. 2014;61.(4)
11. Ross MG, Beall MH. Adult sequelae of intrauterine growth restriction. Semin Perinatol. 2008;32.(3)
12. Kintiraki E, Papakatsika S, Kotronis G, Goulis DG, Kotsis V. Pregnancy-induced hypertension. Hormones (Athens). 2015;14:(2)211-23.
13. Gluhovschi G, Gluhovschi A, Petrica L, Anastasiu D, Gluhovschi C, Velciov S. Pregnancy-induced hypertension--a particular pathogenic model. Similarities with other forms of arterial hypertension. Rom J Intern Med. 2012;50:(1)71-81.
14. Itoh Y, Suzukin Y, Yamamoto T, Konima K, Murakmi I, Suzumon N. Increase in serum concentration of inhibin in early onset preeclampsia with intrauterine growth restriction. J Obstet Gynaecol Res. 2006; 32: 80-5.
15. Ananth CV, Basso O. Impact of pregnancy-induced hypertension on stillbirth and neonatal mortality in fi rst and higher order births: a population-based study. Epidemiology. 2010;21:(1)118-23.
16. . ChaimI SRP, de OliveiraII SMJ, Kimura AF. Pregnancy-induced hypertension and the neonatal outcome. Pregnancy-induced hypertension and the neonatal outcome. Acta paul enferm. 2008; 21:(1)53-8.
17. Muti M, Tshimanga M, Notion GT, Bangure D, Chonzi P. Prevsilence of pregnancy-induced hypertension and pregnancy outcomes among women seeking maternity services in Harare, Zimbabwe. BMC Cardiovasc Disord.2015;15.
18. Gupta KB, Randhawa I, Pal A, Premi HK, Ganeshan J. Perinatal outcome in pregnancy induced hypertension. J Indian Med Assoc.1996;94:(1)6-10.

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