|
 
 |
| REVIEW ARTICLE |
|
| Year : 2017 | Volume
: 15
| Issue : 4 | Page : 262-266 |
|
Risk assessment of intrauterine growth restriction
Reeta Vijayaselvi1, Anne George Cherian2
1 Department of Obstetrics and Gynaecology, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Community Health, Christian Medical College, Vellore, Tamil Nadu, India
| Date of Web Publication | 17-Nov-2017 |
Correspondence Address:
Anne George Cherian
Department of Community Health, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cmi.cmi_76_17
Intrauterine growth restriction is a condition where the estimated fetal weight is less than the 10th percentile on ultrasound and the fetus has not attained its biologically determined growth potential because of a pathologic process. This review deals with the definitions of fetal growth restriction, the etiology associated with it, the types of fetal growth restriction and discusses how to differentiate between them. The various screening mechanisms available, the approach to a patient who is at risk for fetal growth restriction and whether they will benefit from any of the prophylactic measures available are also discussed. Keywords: Estimated fetal weight, fetus in utero, intrauterine growth restriction, small for gestational age
How to cite this article:
Vijayaselvi R, Cherian AG. Risk assessment of intrauterine growth restriction. Curr Med Issues 2017;15:262-6 |
| Introduction | |  |
Intrauterine growth restriction (IUGR) as the name implies is a condition where the fetus has not attained its biologically determined growth potential. The terms “small for gestational age” (SGA) and IUGR are often used interchangeably even though there are subtle differences between the two with implications on how one approaches and treats such a condition. This review deals with the definitions of fetal growth restriction and the etiology associated with it and the types of fetal growth restriction and discusses how to differentiate between them. It is essential that the treating obstetrician identifies IUGR because it has significant implications on the health of the fetus and the mother and is also associated with morbidity and mortality in the perinatal period.
Case Scenario
A 28-year-old female (G2, P1, L1) at 34 weeks of gestation presented to the outpatient department for regular checkup. Her previous baby weighed 2.3 kg at birth. She also had preeclampsia in her previous pregnancy.
What are the investigations you would like to do for her, with the possibility of IUGR at the back of your mind?
| Definitions | | |
Small for gestational age
The definition of small for gestational age for a fetus in utero is an estimated fetal weight that measures less than 10th percentile on ultrasound for that particular gestational age and population. This diagnosis does not necessarily imply pathologic growth abnormalities and may simply describe a fetus at the lower end of the normal range.
It should be noted that 50%–70% of the SGA babies are merely constitutionally small.
Intrauterine growth restriction
Fetal growth restriction or IUGR is defined as fetal growth less than the normal growth potential of a specific infant because of genetic or environmental factors. For a fetus in utero, IUGR refers to a fetus with an estimated fetal weight <10th percentile on ultrasound that, because of a pathologic process, has not attained its biologically determined growth potential.[1] There is often evidence of fetal compromise such as abnormal Doppler studies or decreased liquor volume.
[Figure 1] depicts a growth chart with fetal weight and the 10th and the 90th centiles. | Figure 1: Fetal weight at various gestational ages with 10th centile marked.
Click here to view |
| What is the 10th Centile? | | |
The estimated fetal weight growth chart [Figure 1] plots the estimated weight of the fetus (grams) against the gestational age (weeks) to determine the growth pattern of the child based on a comparison with historical population-based parameters. About 10% of the fetuses fall below the 10th percentile. Historically, the centiles were based on population centiles and these parameters are not uniformly applicable due to wide variations in maternal characteristics across the world. Today, we use centiles customized for maternal characteristics based on maternal height, weight, parity, and ethnic group as well as gestational age at delivery and infant sex. This identifies small babies at higher risk of morbidity and mortality than those identified by population centiles.
| Morbidity and Mortality | | |
IUGR babies have increased risk of perinatal mortality (1.5 times more than general population) and morbidity.[2] Complications such as stillbirth, birth asphyxia, sepsis, necrotizing enterocolitis, intraventricular hemorrhage, meconium aspiration syndrome, hypoglycemia, hypothermia, seizures, and neonatal death are also increased in children with IUGR.[3]
Adult diseases such as hypertension, type 2 diabetes, obesity, coronary artery disease, and hypercholesterolemia are common in these babies. This is known as the Barker hypothesis, more recently named as “fetal origins” or “programming.”[4]
| Etiology | | |
The etiology of IUGR may be broadly classified into maternal causes, fetal causes, and placental causes [Figure 2]. IUGR may be classified into symmetrical and asymmetrical IUGR, both of which have etiologies that are unique to that type [Table 1]. | Table 1: Specific distinctions between symmetric and asymmetric intrauterine growth restriction*
Click here to view |
| Types of Intrauterine Growth Restriction | | |
- Symmetrical IUGR: Symmetrical IUGR is a type of IUGR where all fetal biometric parameters tend to be less than expected (below the 10th percentile) for the given gestational age.[5]
- Asymmetrical IUGR: Asymmetric growth, in which an infant has a smaller abdominal size compared to head size, will occur if the decrease in growth velocity happens in the last trimester. This head-sparing phenomenon is the most common form of IUGR (~70%–80%) and is attributed to the ability of the fetus to adapt, redistributing its cardiac output to the spleen, adrenal, coronary, and cerebral circulations.[4]
| Risk Assessment and Prevention | | |
Risk of recurrence of IUGR in subsequent pregnancies is about 20%.[6] It is therefore important to optimize the maternal condition even before conception as the maternal condition before conception contributes to fetal well-being in many ways. Assessment of the risk of developing IUGR is an important aspect of antenatal care and there are certain features that are associated with a higher risk of IUGR [Table 2].[7] The risk may be evaluated using information obtained from maternal history, laboratory investigations, and ultrasound studies. | Table 2: Risk factors for a small for gestational age neonate (RCOG-green top)
Click here to view |
| History | | |
What are the questions to ask in the maternal history?
- Previous poor obstetric outcomes such as previous intrauterine demises and early neonatal death
- Previous IUGR – There is a 20% chance of recurrence in case of a previous pregnancy with IUGR
- Other risk factors – Preeclampsia, systemic lupus erythematosus, insulin-dependent diabetes, antiphospholipid antibody, heart disease, etc., These conditions predispose the fetus to growth restriction
- Medications such as anticonvulsants, warfarin, and drugs such as alcohol and cocaine increase the mothers' risk for a growth-restricted fetus
- Age – A woman who is more than 35 years of age is at a high-risk factor for growth restriction when compared to younger women.
- Ethnicity – Asian women and African-American women have a tendency to have smaller babies [8]
- Nulliparity
- Low prepregnancy body mass index
- Heavy first trimester bleeding.
| Laboratory Investigations | | |
Serum levels of pregnancy-associated plasma protein A (PAPP-A) expressed in multiple of median (MoM) may point to a possible IUGR. A systematic review found that an unexplained low first-trimester PAPP-A (<0.4 MoM) was associated with an increased frequency of adverse obstetrical outcome including an SGA infant.[9]
| Ultrasound Studies | | |
Uterine artery Doppler – Uterine artery Doppler is done at 20–24 weeks of GA for the women having high risk for SGA. Abnormal Doppler, i.e., increased pulsatility index (PI >95th centile) with/without diastolic notching can also be a predictor for SGA. If there is abnormal Doppler, there must be close surveillance from 26 to 28 weeks. Predictive value improves when PAPP-A is added. Uterine artery Doppler studies are used for screening only in women having a high risk for SGA [Figure 3].
| Management of Those With High Risk for Intrauterine Growth Restriction | | |
In mothers who have been identified to have high-risk factors for IUGR, certain measures may be initiated to prevent the possibility of growth restriction in the fetus.
| Role of Aspirin | | |
There is adequate evidence from several meta-analyses and controlled trials, which has shown that low-dose aspirin reduces the risk of pregnancy-induced hypertension and IUGR in women at high risk of these disorders.[10] Aspirin must be started as early as possible and before 12 weeks of gestation in all pregnancies with risk factors for IUGR and continued till 36 weeks at a dose of 1–2 mg/kg/day (75–150 mg).
Meta-analysis of 27 studies shows that aspirin when started before 16 weeks significantly reduces IUGR, preeclampsia, and preterm birth.[11] The NICE guidelines identify certain risk factors where aspirin is to be started and may have a beneficial effect [Table 3].[12] | Table 3: National Institute for Health and Care Excellence guidelines for initiating aspirin
Click here to view |
| How Does Aspirin Act? | | |
The anti-inflammatory action of aspirin is considered to be the underlying mechanism for the beneficial effect in preventing preeclampsia and IUGR. The most recognized mechanism of action of aspirin is to inhibit the synthesis of prostaglandins, but this by itself does not explain the repertoire of anti-inflammatory effects of aspirin. Later, another mechanism was described: the induction of the production of aspirin-triggered lipoxins (ATLs) from arachidonic acid by acetylation of the enzyme cyclooxygenase-2. It has been found that, similar to endogenously produced lipoxins, ATL resolves inflammation and acts as antioxidant and immunomodulator. In preeclampsia, IUGR and in the obstetric antiphospholipid syndrome, there is thought to be an underlying inflammatory process and the role of aspirin might be based on the induction of ATL.[13]
| Other Measures to Reduce Risk | | |
Cessation of smoking is also advised to women who are smokers. If stopped before 15 weeks of gestation, the outcome is similar to nonsmokers.
There are certain practices which have not been proven to be beneficial once diagnosed with IUGR. These are bed rest, progesterone supplementation, and nutritional supplementation.
| Conclusion | | |
IUGR is associated with increased perinatal mortality and morbidity. Early-onset or symmetrical IUGR is usually due to chromosomal abnormality or infection, while late-onset or asymmetrical IUGR is due to uteroplacental insufficiency.
Aspirin plays a significant role in the prevention of recurrence of IUGR and preeclampsia. Uterine artery Doppler abnormality predicts IUGR and is useful only in high-risk women. Once IUGR is identified, close surveillance is done to prevent its complications.
Answer to case scenario
As the patient has had a previous baby with IUGR, she has a high chance of recurrence and must be closely monitored for growth restriction. She must have an ultrasound done to determine fetal growth and weight. She must then be followed up closely, as discussed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Lausman A, Kingdom J, Maternal Fetal Medicine Committee. Intrauterine growth restriction: Screening, diagnosis, and management. J Obstet Gynaecol Can 2013;35:741-8.  |
| 2. | Mandruzzato G, Antsaklis A, Botet F, Chervenak FA, Figueras F, Grunebaum A, et al. Intrauterine restriction (IUGR). J Perinat Med 2008;36:277-81. [ PUBMED] |
| 3. | Sharma D, Sharma P, Shastri S. Postnatal complications of intrauterine growth restriction. J Neonatal Biol 2016;5:1-8. |
| 4. | Militello M, Pappalardo EM, Ermito S, Dinatale A, Cavaliere A, Carrara S, et al. Obstetric management of IUGR. J Prenat Med 2009;3:6-9. |
| 5. | Peleg D, Kennedy CM, Hunter SK. Intrauterine growth restriction; Identification and management. Am Fam Physician 1998;58:453-60. [ PUBMED] |
| 6. | Voskamp BJ, Kazemier BM, Ravelli AC, Schaaf J, Mol BW, Pajkrt E, et al. Recurrence of small-for-gestational-age pregnancy: Analysis of first and subsequent singleton pregnancies in the Netherlands. Am J Obstet Gynecol 2013;208:374.e1-6. |
| 7. | |
| 8. | |
| 9. | Morris RK, Cnossen JS, Langejans M, Robson SC, Kleijnen J, Ter Riet G, et al. Serum screening with down's syndrome markers to predict pre-eclampsia and small for gestational age: Systematic review and meta-analysis. BMC Pregnancy Childbirth 2008;8:33. [ PUBMED] |
| 10. | Low-dose aspirin in prevention and treatment of intrauterine growth retardation and pregnancy-induced hypertension. Italian study of aspirin in pregnancy. Lancet 1993;341:396-400. [ PUBMED] |
| 11. | Bujold E, Roberge S, Lacasse Y, Bureau M, Audibert F, Marcoux S, et al. Prevention of preeclampsia and intrauterine growth restriction with aspirin started in early pregnancy: A meta-analysis. Obstet Gynecol 2010;116:402-14. [ PUBMED] |
| 12. | |
| 13. | Cadavid AP. Aspirin: The mechanism of action revisited in the context of pregnancy complications. Front Immunol 2017;8:261. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]
| This article has been cited by | | 1 |
The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease |
|
| Miguel A. Ortega, Oscar Fraile-Martínez, Cielo García-Montero, Miguel A. Sáez, Miguel Angel Álvarez-Mon, Diego Torres-Carranza, Melchor Álvarez-Mon, Julia Bujan, Natalio García-Honduvilla, Coral Bravo, Luis G. Guijarro, Juan A. De León-Luis | | Cells. 2022; 11(3): 568 | | [Pubmed] | [DOI] | | | 2 |
A systematic review on estimating population attributable fraction for risk factors for small-for-gestational-age births in 81 low- and middle-income countries |
|
| Sabi Gurung, Hannah Hanzi Tong, Emily Bryce, Joanne Katz, Anne CC Lee, Robert E Black, Neff Walker | | Journal of Global Health. 2022; 12 | | [Pubmed] | [DOI] | | | 3 |
CD68+ M1 MACROPHAGES IS ASSOCIATED WITH PLACENTAL INSUFFICIENCY UNDER FETAL GROWTH RESTRICTION |
|
| Varvara A. Berezhna,Tetiana V. Mamontova,Antonina M. Gromova | | Wiadomosci Lekarskie. 2021; 74(2): 213 | | [Pubmed] | [DOI] | | | 4 |
Maternal Serum Copeptin As a Biomarker For Intrauterine Growth Restriction |
|
| Amber Hassan, Hisham Nasief | | Pakistan BioMedical Journal. 2021; 4(2) | | [Pubmed] | [DOI] | | | 5 |
Maternal high fat diet-induced obesity affects trophoblast differentiation and placental function in mice† |
|
| Tobias Kretschmer,Eva-Maria Turnwald,Ruth Janoschek,Peter Zentis,Inga Bae-Gartz,Tim Beers,Marion Handwerk,Maria Wohlfarth,Mojgan Ghilav,Wilhelm Bloch,Eva Hucklenbruch-Rother,Jörg Dötsch,Sarah Appel | | Biology of Reproduction. 2020; | | [Pubmed] | [DOI] | | | 6 |
THE ROLE OF GYNECOLOGICAL DISEASES IN THE INTRAUTERINE GROWTH RETARDATION |
|
| A. M. Gromova,V. A. Berezhna | | Bulletin of Problems Biology and Medicine. 2020; 1(1): 116 | | [Pubmed] | [DOI] | | | 7 |
Knowledge Gaps and Emerging Research Areas in Intrauterine Growth Restriction-Associated Brain Injury |
|
| Bobbi Fleiss,Flora Wong,Fiona Brownfoot,Isabelle K. Shearer,Olivier Baud,David W. Walker,Pierre Gressens,Mary Tolcos | | Frontiers in Endocrinology. 2019; 10 | | [Pubmed] | [DOI] | | | 8 |
Regulation of Placental Development and Its Impact on Fetal Growth—New Insights From Mouse Models |
|
| Laura Woods,Vicente Perez-Garcia,Myriam Hemberger | | Frontiers in Endocrinology. 2018; 9 | | [Pubmed] | [DOI] | |
|
 |
|
|
|
Search Pubmed for