IUGR

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intrauterine growth restriction IUGR etiology classification pathophysiology

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IUGR diagnosis surveillance management fetal monitoring

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IUGR fetal Doppler umbilical artery waveform

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small for gestational age SGA fetal growth restriction causes maternal fetal placental

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fetal growth restriction Doppler biophysical profile delivery timing neonatal outcome

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Intrauterine Growth Restriction (IUGR)

Definition & Classification

IUGR refers to a fetus that fails to reach its genetically predetermined growth potential, typically defined as an estimated fetal weight (EFW) or abdominal circumference (AC) < 10th percentile for gestational age on ultrasound, with evidence of a pathological process (distinguishing it from constitutional smallness).
TermDefinition
SGA (Small for Gestational Age)Birth weight < 10th percentile; may be constitutional
IUGRPathological failure to reach growth potential (< 10th percentile + Doppler/functional compromise)
Severe IUGREFW < 3rd percentile
Two phenotypes:
  • Symmetric IUGR (~20–30%): All parameters reduced proportionally; onset early (< 28 wks); often fetal/chromosomal cause
  • Asymmetric IUGR (~70–80%): Head-sparing with reduced abdominal circumference; onset late; typically placental/uteroplacental insufficiency

Etiology

Maternal (~25–30%)

  • Hypertensive disorders (preeclampsia, chronic hypertension)
  • Diabetes with vascular disease
  • Autoimmune conditions (antiphospholipid syndrome, SLE)
  • Chronic renal disease
  • Severe anemia, malnutrition, underweight
  • Smoking, alcohol, cocaine use
  • PCOS (OR ~1.77 vs. non-PCOS pregnancies; Assessment and Management of PCOS, p. 136)
  • Thrombophilias

Placental (~40%)

  • Placental insufficiency / uteroplacental insufficiency (most common)
  • Placenta previa, abruption
  • Velamentous cord insertion
  • Circumvallate placenta

Fetal (~15%)

  • Chromosomal anomalies (trisomy 13, 18, 21; Turner syndrome)
  • Structural congenital anomalies
  • Inborn errors of metabolism
  • Multiple gestation (twin-twin transfusion)

Infectious (~5–10%)

  • TORCH infections: Toxoplasma, Other (syphilis, VZV, parvovirus B19), Rubella, CMV, Herpes

Pathophysiology

The final common pathway is reduced oxygen and nutrient delivery to the fetus:
  1. Defective trophoblast invasion → inadequate spiral artery remodeling
  2. Increased placental vascular resistance → ↑ umbilical artery pulsatility
  3. Fetal redistribution response: vasodilation of cerebral/coronary/adrenal circulation ("brain-sparing" = ↓ MCA resistance)
  4. Progressive decompensation: absent/reversed end-diastolic flow (AEDF/REDF) in umbilical artery → venous pulsations in ductus venosus → fetal death

Diagnosis

Screening

  • Uterine artery Doppler at 20–24 weeks (↑ PI / notching predicts placental insufficiency)
  • Serial symphysis-fundal height (SFH) measurements — flattening or lag triggers ultrasound

Ultrasound Biometry

  • Abdominal circumference (AC) — most sensitive single parameter
  • EFW < 10th percentile (severe < 3rd percentile)
  • Serial measurements every 2–4 weeks to assess growth velocity (crossing centiles is as important as absolute value)

Doppler Studies (key for surveillance & timing)

Progressive umbilical artery Doppler abnormalities in IUGR — from reduced diastolic flow (a), to absent end-diastolic flow (b), to reversed end-diastolic flow (c), indicating worsening placental resistance
Doppler VesselFindingSignificance
Umbilical artery (UA)↑ PI / S:D ratioPlacental resistance
UAAbsent end-diastolic flow (AEDF)High risk — consider delivery
UAReversed end-diastolic flow (REDF)Imminent deterioration — urgent delivery
Middle cerebral artery (MCA)↓ PI (brain-sparing)Cerebrovascular redistribution
Cerebroplacental ratio (CPR)< 1Independent predictor of adverse outcome
Ductus venosus (DV)Absent/reversed A-wavePre-terminal; delivery indicated

Biophysical Profile (BPP)

  • Scores fetal tone, movement, breathing, amniotic fluid, and NST (0–10)
  • Score ≤ 4: high risk of acidosis, consider delivery
  • Score 6: repeat in 4–6 hours

Management

Antepartum

  • Identify and treat underlying cause (e.g., optimize BP in hypertension, treat infection)
  • Aspirin (low-dose, 100–150 mg/day from 11–14 weeks): reduces risk of placental IUGR in high-risk women
  • No proven intervention improves growth directly once IUGR is established
  • Optimize maternal nutrition, stop smoking/drugs
  • Corticosteroids if preterm delivery anticipated (< 34 weeks)
  • Magnesium sulfate for neuroprotection if < 32 weeks

Surveillance Frequency

SeverityUA DopplerBPP/NSTGrowth USS
EFW < 10th, normal DopplerEvery 2 weeksWeeklyEvery 2–4 weeks
Abnormal UA PI, normal diastoleTwice weeklyTwice weeklyEvery 2 weeks
AEDF2–3× weeklyDaily BPPEvery 1–2 weeks
REDFDailyDaily
Abnormal DVDeliver

Timing of Delivery

Gestational AgeIndicationRecommended Action
≥ 37 weeksAny IUGRDeliver
34–37 weeksAEDF, deteriorating BPPConsider delivery
32–34 weeksREDF, BPP ≤ 4Deliver after steroids
< 32 weeksAbnormal DV, BPP ≤ 4Deliver (balance prematurity risk)
ACOG recommends delivery at 36–37 weeks for most cases of placental IUGR.

Mode of Delivery

  • Vaginal delivery is acceptable if no acute compromise
  • Continuous electronic fetal monitoring in labor is mandatory
  • Low threshold for cesarean section with abnormal Dopplers (AEDF/REDF) or non-reassuring CTG

Complications

Perinatal

  • Stillbirth / intrauterine fetal demise (IUFD)
  • Birth asphyxia, meconium aspiration
  • Hypoglycemia, hypothermia, polycythemia
  • Necrotizing enterocolitis (NEC)
  • Respiratory distress syndrome (prematurity)
  • Neurodevelopmental impairment

Long-term (Barker Hypothesis / Fetal Origins of Adult Disease)

  • Hypertension, coronary artery disease
  • Type 2 diabetes / insulin resistance
  • Obesity
  • SGA is associated with ↑ risk of hypertension and diabetes in the offspring (Management of CVD and Pregnancy, p. 78)

Key Points Summary

  • IUGR ≠ SGA — IUGR implies pathological growth failure confirmed by Doppler/functional compromise
  • Placental insufficiency is the most common cause in developed countries
  • Umbilical artery Doppler is the cornerstone of surveillance — AEDF/REDF are delivery triggers
  • No treatment restores normal fetal growth; management is surveillance + timely delivery
  • Long-term cardiovascular and metabolic risks are significant for both mother and offspring
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