Guideline 13.4 — Fetal Growth Restriction & Placental Insufficiency

BEDSIDE ACTION BOX — The Growth-Restricted Newborn

Anticipate the classic quartet at birth: perinatal hypoxia, hypothermia, hypoglycemia, and polycythemia.
Warm aggressively (little fat) and feed early with close glucose monitoring (little glycogen).
Check a venous hematocrit if plethoric or symptomatic; watch bilirubin as the red-cell mass turns over.
In early, symmetric growth restriction without a placental explanation, think congenital infection (TORCH) and aneuploidy.
Abnormal umbilical artery Dopplers (absent/reversed end-diastolic flow) flag the highest-risk fetuses — know the antenatal picture.

1. Overview & Definition

Definition

Fetal growth restriction (FGR) describes a fetus that fails to reach its genetically determined growth potential, most often because of placental insufficiency. It overlaps with — but is not identical to — "small for gestational age" (SGA), a purely statistical label (birth weight below the 10th centile). A constitutionally small but healthy baby is SGA without being growth-restricted; a pathologically starved fetus is growth-restricted even if just above the 10th centile.

Why This Topic Matters

The growth-restricted infant has thin reserves and a placenta that has been failing — so the delivery room and first hours carry predictable risks. Recognizing the pattern lets you pre-empt hypoxia, cold, low sugar, and hyperviscosity rather than chase them.

2. Who This Guideline Applies To

Scope

Infants identified antenatally or at birth as growth-restricted or SGA.
Infants of pregnancies complicated by placental insufficiency, hypertensive disease, or abnormal Doppler studies.
Cross-references: preeclampsia (13.2); congenital infection (8.x); polycythemia (10.x); hypoglycemia (4.x); dysmorphology/aneuploidy (12.x).

3. Symmetric vs Asymmetric Growth Restriction

	Symmetric FGR	Asymmetric FGR
Timing of insult	Early (first/second trimester)	Later (third trimester)
Pattern	Head, length, and weight all reduced proportionately	"Head-sparing" — weight down more than head circumference
Typical cause	Intrinsic: aneuploidy, congenital infection, genetic syndromes, teratogens	Extrinsic: placental insufficiency (e.g., preeclampsia)
Prognosis clue	Depends on underlying cause	Usually catches up with good nutrition if cause resolves

4. Causes & Risk Factors

Think in Three Buckets

Maternal/placental: hypertensive disease/preeclampsia, chronic disease, smoking, substance use, poor nutrition, placental abnormalities.
Fetal: aneuploidy and genetic syndromes, congenital infection (TORCH — CMV especially), multiple gestation.
Uteroplacental blood flow: abnormal spiral-artery remodeling → the Doppler abnormalities seen antenatally.

5. Clinical Presentation

What You See at the Bedside

Thin infant with loose skin, reduced subcutaneous fat and muscle, and (in asymmetric FGR) a relatively normal head size.
Signs of perinatal compromise if the placenta failed acutely (low Apgars, meconium, acidosis).
Plethora if polycythemic; jitteriness if hypoglycemic or polycythemic.
Features suggesting an intrinsic cause: dysmorphism, microcephaly, hepatosplenomegaly, petechiae, or a "blueberry-muffin" rash (congenital infection).

6. Recommended Workup

What to Check

Glucose: screen for hypoglycemia per the at-risk protocol — a top priority in FGR.
Temperature: active thermoregulation from birth.
Hematocrit: venous sample to screen for polycythemia; monitor bilirubin.
If intrinsic cause suspected (symmetric, dysmorphic, no placental explanation): congenital infection screen (including CMV), and consider genetic testing/microarray with genetics involvement.
Examination: careful head-to-toe for dysmorphism and anomalies.

7. Delivery-Room & First-Hours Plan

Anticipate

Review growth trajectory and Doppler studies; prepare for possible perinatal depression and meconium.

Resuscitate and warm

Standard NRP; aggressive thermoregulation because fat stores are low.

Protect glucose

Feed early or start IV dextrose; monitor glucose closely — glycogen reserves are minimal.

Screen hematocrit

Check venous Hct if plethoric/symptomatic; hydrate; monitor bilirubin.

Determine the cause

If symmetric/dysmorphic with no placental explanation, pursue infection and genetic work-up.

8. Management of the Associated Problems

Problem	Approach
Hypothermia	Warm environment, skin-to-skin/incubator, minimize heat loss from birth.
Hypoglycemia	Early feeds; IV dextrose for significant/symptomatic lows; monitor closely and wean slowly.
Polycythemia / hyperviscosity	Hydration; partial exchange transfusion only for symptomatic, very high hematocrit.
Hyperbilirubinemia	Phototherapy on the nomogram; anticipate higher loads with polycythemia.
Perinatal hypoxia	Standard supportive/neuroprotective care; assess for HIE if indicated.
Intrinsic cause (infection/genetic)	Directed treatment and counseling with the relevant specialties.

9. Monitoring

What to Track

Glucose and temperature until stable on feeds.
Hematocrit and bilirubin as indicated.
Growth (weight, length, head circumference) and feeding tolerance — expect catch-up in asymmetric FGR.

10. Contraindications & Precautions

Safety Cautions

Do not assume every small baby is simply constitutionally small — distinguish SGA from pathological FGR.
Do not overlook a congenital-infection or genetic cause in early, symmetric growth restriction.
Do not under-treat hypothermia and hypoglycemia — reserves are minimal.
Do not perform partial exchange transfusion for an asymptomatic, borderline hematocrit.

11. Escalation & Follow-Up

Escalate When…

Refractory hypoglycemia, symptomatic polycythemia, or signs of hypoxic-ischemic injury.
Suspected congenital infection or a genetic/syndromic diagnosis.
Poor feeding or failure to establish catch-up growth.

Discharge & Follow-Up

Stable glucose and temperature on feeds; establishing weight gain.
Growth and neurodevelopmental follow-up — FGR carries longer-term risks of neurodevelopmental impairment and adult metabolic disease (fetal programming).
Directed specialty follow-up if an intrinsic cause was found.

Parent Counselling Points

"Your baby was smaller than expected because the placenta wasn't delivering as much as it should. In the first days we focus on warmth, feeding, and blood sugar."
"Many of these babies catch up their growth once feeding is going well; we'll keep an eye on growth and development over time."
"Sometimes we look for a specific cause, such as an infection during pregnancy, so the tests you see are part of understanding why."

12. Key Pearls

High-Value Clinical Pearls

SGA is a statistic; FGR is a pathology — they overlap but are not the same.
Asymmetric (head-sparing) = late placental cause; symmetric = early intrinsic cause (infection, aneuploidy).
The birth quartet to pre-empt: hypoxia, hypothermia, hypoglycemia, polycythemia.
Absent/reversed umbilical artery end-diastolic flow marks the highest-risk fetuses.
CMV is the classic congenital infection behind symmetric FGR with microcephaly.

13. Common Mistakes to Avoid

Pitfalls & Better Practice

The recurring errors in caring for the growth-restricted infant.

Mistake	Why it harms	Better practice
Treating all SGA infants as pathological (or none as pathological).	Misclassifies risk.	Distinguish constitutional SGA from true FGR.
Missing hypoglycemia/hypothermia.	Low reserves decompensate fast.	Warm and feed early; monitor glucose.
Ignoring an intrinsic cause in symmetric FGR.	Misses infection/aneuploidy.	Screen for TORCH and consider genetics.
Over-treating a borderline hematocrit.	Unnecessary invasive procedure.	Partial exchange only if symptomatic and very high.

14. Board-Style High-Yield Summary

Key Takeaways

FGR = failure to reach growth potential, usually from placental insufficiency; SGA is the statistical (<10th centile) label.
Symmetric FGR → early intrinsic cause (aneuploidy, congenital infection); asymmetric (head-sparing) → late placental cause.
At birth: pre-empt perinatal hypoxia, hypothermia, hypoglycemia, and polycythemia/hyperviscosity.
Abnormal umbilical artery Dopplers (absent/reversed EDF) mark the highest antenatal risk.
Long term: neurodevelopmental risk and adult metabolic disease (fetal programming).

15. References

1.American College of Obstetricians and Gynecologists. Fetal Growth Restriction. ACOG Practice Bulletin.
2.Society for Maternal-Fetal Medicine. Diagnosis and management of fetal growth restriction.
3.Baylor College of Medicine, Division of Neonatology. Guidelines for Acute Care of the Neonate, Edition 33, 2025–2026.
4.Gomella TL, et al. Neonatology: Management, Procedures, On-Call Problems — Intrauterine Growth Restriction.

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Chapter 13.4 — Fetal Growth Restriction & Placental Insufficiency