Intrauterine Growth Restriction

Granny maureenb bankie69485 weenett 676 Users are discussing this topic

PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Synonyms: IUGR, fetal growth restriction, FGR

Intrauterine growth restriction (IUGR) is a condition where a baby's growth slows or ceases when it is in the uterus.

It is part of a wider group - small for gestational age (SGA) fetuses - which includes fetuses that have failed to achieve their growth potential and fetuses that are constitutionally small.

Approximately 50-70% of fetuses with a birth weight below the tenth centile for gestational age are constitutionally small. The lower the centile for defining SGA, the greater the likelihood of IUGR. On the other hand, a fetus with growth restriction may not be SGA.[1] 

NEW - log your activity

  • Notes
    Add notes to any clinical page and create a reflective diary
  • Track
    Automatically track and log every page you have viewed
  • Print
    Print and export a summary to use in your appraisal
Click to find out more »

There is increased risk of:

  • Intrapartum fetal distress
  • Intrapartum asphyxia
  • Postnatal hypoglycaemia or hypocalcaemia neonatal complications
  • Impaired neurodevelopment
  • Meconium aspiration
  • Intrauterine death
  • Possibly type 2 (non insulin-dependent) diabetes and hypertension in adult life

The risk assessment must always be individualised and take into account the previous medical and obstetric history and current pregnancy history. The progression of a disease or starting medical treatment may increase the risk. The following are risk factors to be considered at the time of the booking assessment in the first trimester.[1] 

Major risk factors

  • Maternal age over 40 years; smoker of 11 cigarettes or more per day; cocaine use; daily vigorous exercise
  • Previous SGA baby; previous stillbirth
  • Maternal SGA
  • Chronic hypertension, diabetes and vascular disease, renal impairment, antiphospholipid syndrome
  • Heavy bleeding similar to menstrual periods
  • Fetal echogenic bowel
  • Pre-eclampsia, severe pregnancy-induced hypertension, unexplained antepartum haemorrhage, low maternal weight
  • Pregnancy-associated plasma protein A (PAPP-A); a low level of the first trimester marker PAPP-A is a major risk factor for delivery of an SGA neonate.

Minor risk factors

  • Maternal age 35 years or older; nulliparity; BMI <20; BMI 25-29.9; smokes 1-10 cigarettes per day; low fruit intake pre-pregnancy
  • Pregnancy interval less than six months; pregnancy interval 30 months or greater
  • Paternal SGA
  • When the problem is placental insufficiency, the head is not as restricted in size as the abdominal girth - head sparing. This represents preferential nutrition to the brain, with a lack of glycogen stored in the liver.
  • If there is a fetal problem such as a chromosome abnormality, there is uniform restriction of growth.

There may be racial differences. Babies of Indian race tend to be a little smaller. If the fetus is in the lower centiles but continues to grow within those centiles, this is reassuring but if growth is slow and the fetus is falling into lower centiles, this is cause for concern.

  • Fetal abdominal circumference (AC) or estimated fetal weight (EFW) <10th centile can be used to diagnose an SGA fetus. Use of a customised fetal weight reference may improve prediction of an SGA neonate and perinatal outcome.
  • When using two measurements of AC or EFW to estimate growth velocity, they should be at least three weeks apart to minimise false positive rates for diagnosing IUGR.
  • Where the fetal AC or EFW is <10th centile or there is evidence of reduced growth velocity, women should be offered serial assessment of fetal size and umbilical artery Doppler scan.

In a high-risk population, the use of umbilical artery Doppler scan has been shown to reduce perinatal morbidity and mortality. Umbilical artery Doppler scan should be the primary surveillance tool in the SGA fetus.

  • All women should be assessed at booking for risk factors for an SGA fetus/neonate to identify those who require increased surveillance.
  • If there is one major risk factor or three or more minor risk factors (see 'Risk factors', above) found at the booking assessment, then the woman should be reassessed at 20 weeks for abnormal Down's syndrome markers (minor risk factor) and fetal echogenic bowel (major risk factor).
  • If there are one or more risk factors following the reassessment at 20 weeks of gestation, then serial assessment of fetal size and umbilical artery Doppler scan are required from 26-28 weeks of pregnancy.
  • Women who have three or more minor risk factors should be referred for uterine artery Doppler scan at 20-24 weeks of gestation:
    • Women with an abnormal uterine artery Doppler scan at 20-24 weeks should be referred for serial ultrasound measurement of fetal size and assessment of well-being with umbilical artery Doppler scan commencing at 26-28 weeks of pregnancy.
    • Women with a normal uterine artery Doppler scan do not require serial measurement of fetal size and serial assessment of well-being with umbilical artery Doppler scan unless they develop specific pregnancy complications - eg, antepartum haemorrhage or hypertension. However, they should be offered a scan for fetal size and umbilical artery Doppler scan during the third trimester.
  • Serial ultrasound measurement of fetal size and assessment of well-being with umbilical artery Doppler scan should be offered in cases of fetal echogenic bowel.

When umbilical artery Doppler flow indices are normal it is reasonable to repeat surveillance every 14 days. More frequent Doppler surveillance may be appropriate in severe SGA and also when umbilical artery Doppler flow indices are abnormal and delivery is not indicated.

Cardiotocography (CTG) should not be used as the only form of surveillance in SGA fetuses. Interpretation of the CTG should be based on short-term fetal heart rate variation from computerised analysis.

Ultrasound assessment of amniotic fluid volume should not be used as the only form of surveillance in SGA fetuses.

Abdominal palpation has limited accuracy for the prediction of an SGA neonate and thus should not be routinely performed in this context. Serial measurement of symphysis fundal height (SFH) is recommended at each antenatal appointment from 24 weeks of pregnancy, as this improves prediction of an SGA neonate.

SFH should be plotted on a customised rather than a population-based chart, as this may improve prediction of an SGA neonate. Women with a single SFH which plots below the 10th centile or serial measurements which demonstrate slow or static growth by crossing centiles should be referred for ultrasound measurement of fetal size.

Women in whom measurement of SFH is inaccurate (eg, BMI >35, large fibroids, hydramnios) should be referred for serial assessment of fetal size using ultrasound.

The use of Doppler ultrasonography to measure umbilical artery waveforms should be considered a part of fetal evaluation once IUGR is suspected or diagnosed. The ultrasound criteria for IUGR include:

  • An elevated ratio of femoral length to abdominal circumference (AC)
  • An elevated ratio of head circumference (HC) to AC
  • Unexplained oligohydramnios

Other investigations include:[1] 

  • Detailed fetal anatomical survey and uterine artery Doppler by a fetal medicine specialist if severe SGA is identified at the 18- to 20-week scan.
  • Karyotyping for severely SGA fetuses with structural anomalies and in those detected before 23 weeks of gestation, especially if uterine artery Doppler scan is normal.
  • Serological screening for congenital cytomegalovirus (CMV) and toxoplasmosis infection for severely SGA fetuses.
  • Testing for syphilis and malaria in high-risk populations.

Interventions to be considered in the preterm SGA fetus

Women with an SGA fetus between 24+0 and 35+6 weeks of gestation where delivery is being considered should receive a single course of antenatal corticosteroids.[2]  

When to deliver an SGA fetus

In the term SGA fetus with normal umbilical artery Doppler scan, an abnormal middle cerebral artery Doppler scan has moderate predictive value for acidosis at birth and should be used to time delivery. Ductus venosus Doppler scan has moderate predictive value for acidaemia and adverse outcome. Ductus venosus Doppler scan should be used for surveillance in the preterm SGA fetus with abnormal umbilical artery Doppler scan and used to time delivery.

In the preterm SGA fetus with umbilical artery absent or reversed end-diastolic velocity (AREDV) detected prior to 32 weeks of gestation, delivery is recommended when ductus venosus Doppler scan becomes abnormal or umbilical vein pulsations appear, provided the fetus is considered viable, and after completion of steroids. Even when venous Doppler scan is normal, delivery is recommended by 32 weeks of gestation and should be considered between 30-32 weeks of gestation.

If middle cerebral artery Doppler scan is abnormal, delivery should be recommended no later than 37 weeks of gestation.

In the SGA fetus detected after 32 weeks of gestation with an abnormal umbilical artery Doppler scan, delivery no later than 37 weeks of gestation is recommended.

In the SGA fetus detected after 32 weeks of gestation with normal umbilical artery Doppler scan, a senior obstetrician should be involved in determining the timing and mode of birth of these pregnancies. Delivery should be offered at 37 weeks of gestation.

Method of delivery

  • In the SGA fetus with umbilical artery AREDV, delivery by caesarean section is recommended.
  • In the SGA fetus with normal umbilical artery Doppler scan or with abnormal umbilical artery pulsatility index but end-diastolic velocities present, induction of labour can be offered but rates of emergency caesarean section are increased and continuous fetal heart rate monitoring is recommended from the onset of uterine contractions.

Early admission is recommended in women in spontaneous labour with an SGA fetus in order to instigate continuous fetal heart rate monitoring.[3]

  • Babies who have been starved in utero tend to be hungry and feed enthusiastically to gain weight. As an adult they can expect normal or only slightly reduced stature.
  • If there was slow head growth before 26 weeks they may show significant developmental delays at 4 years of age. It has also been shown to be associated with impaired executive cognitive function in young adults.[4]
  • An extremely low birth weight implies a high risk of perinatal mortality and neonatal morbidity, but the most significant variable that can be correlated to the long-term neurological outcome is the gestational age.[5]
  • Studies have shown that infants with birth weight below 2.5 kg have a three times increased risk of death due to coronary artery disease later in life.[6] There seems to be an increased risk of hypertension,[7] type 2 diabetes,[8] and autoimmune thyroid disease.
  • Antiplatelet agents may be effective in preventing SGA in women at high risk of pre-eclampsia although the effect size is small.
  • In women at high risk of pre-eclampsia, antiplatelet agents should be commenced at, or before, 16 weeks of pregnancy.
  • There is no consistent evidence that dietary modification, progesterone or calcium prevents SGA.
  • Interventions to promote smoking cessation may prevent SGA and should be offered to all pregnant women who smoke.
  • Antithrombotic therapy appears to be a promising therapy for preventing SGA in high-risk women. However, there is insufficient evidence, especially concerning serious adverse effects, to recommend its use.

Further reading & references

  1. Small-for-Gestational-Age Fetus, Investigation and Management; Royal College of Obstetricians and Gynaecologists Green top guideline (Mar 2013)
  2. Antenatal Corticosteroids to Reduce Neonatal Morbidity and Mortality; Royal College of Obstetricians and Gynaecologists (October 2010)
  3. Intrapartum care; NICE Clinical Guideline (2007)
  4. Tideman E, Marsal K, Ley D; Cognitive function in young adults following intrauterine growth restriction with abnormal fetal aortic blood flow. Ultrasound Obstet Gynecol. 2007 Jun;29(6):614-8.
  5. Valcamonico A, Accorsi P, Sanzeni C, et al; Mid- and long-term outcome of extremely low birth weight (ELBW) infants: An analysis of prognostic factors. J Matern Fetal Neonatal Med. 2007 Jun;20(6):465-71.
  6. Gortner L; Intrauterine growth restriction and risk for arterial hypertension: a causal relationship? J Perinat Med. 2007 Jul 12;.
  7. Shankaran S, Das A, Bauer CR, et al; Fetal origin of childhood disease: intrauterine growth restriction in term infants and risk for hypertension at 6 years of age. Arch Pediatr Adolesc Med. 2006 Sep;160(9):977-81.
  8. Jansson T, Powell TL; Role of the placenta in fetal programming: underlying mechanisms and potential interventional approaches. Clin Sci (Lond). 2007 Jul;113(1):1-13.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Peer Reviewer:
Dr John Cox
Document ID:
2336 (v23)
Last Checked:
Next Review:

Did you find this health information useful?

Yes No

Thank you for your feedback!

Subcribe to the Patient newsletter for healthcare and news updates.

We would love to hear your feedback!

Patient Access app - find out more Patient facebook page - Like our page