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Key messages

  • Outcomes for small for gestational age (SGA) infants are principally determined by cause.
  • Symmetrical SGA indicates slow development through the pregnancy and brain growth may be limited.
  • In asymetrical SGA infants head circumference and length are relatively well preserved; brain growth is relatively spared.
  • Investigations may be required to establish the cause of growth restriction.
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    Please note that all guidance is currently under review and some may be out of date. We recommend that you also refer to more contemporaneous evidence in the interim.

    Small for gestational age (SGA) infants are defined as having a birthweight more than 2SD below the mean or less than the 10th percentile for the gestational age.

    Infants whose weight is greater than the 10th percentile but who are thin relative to their length and head circumference are at similar risk of neonatal complications as SGA infants.

    Types of SGA

    Symmetric

    Characteristics of symmetric SGA include:

    • weight, head circumference and length all below the 10th percentile
    • slow development throughout the pregnancy
    • limited brain growth.

    Causes of symmetric SGA include:

    • chromosomal abnormalities
    • intrauterine infection
    • severe placental insufficiency
    • constitutionally small infant.

    Asymmetric

    Characteristics of asymmetric SGA include:

    • weight below the 10th percentile
    • head circumference and length relatively preserved
    • fetus has grown normally for first two trimesters
    • brain growth relatively spared.

    Causes of asymmetric SGA include:

    • interference with placental function
    • interference with maternal health in third trimester.

    Infants whose weight is greater than the 10th percentile but who are thin relative to their length and head circumference are at similar risk of neonatal complications as SGA infants.

    They should be considered ‘relatively’ SGA (Clifford syndrome).

    The weight/length ratio (Ponderal Index = [weight (g)]/[length (cm)]3 ) is less than normal for such infants.

    However, unless great care is taken with the measurement of length the calculated index can be misleading.

    Aetiology

    Fetal
    • Chromosome disorders: (Trisomy 21, 18, 13)
    • Chronic congenital infection: (CMVrubellasyphilistoxoplasmosis)
    • Congenital malformations: congenital heart disease, diaphragmatic hernia, tracheo-oesophageal fistula
    • Syndrome complex
    • Radiation
    • Multiple gestation relates more to placental limitation rather than intrinsic baby problem
     Maternal
    • Pregnancy induced hypertension
    • Hypertension, renal disease, or both
    • Hypoxaemia (high altitude, cyanotic cardiac or pulmonary disease)
    • Malnutrition or chronic illness
    • Drugs (narcotics, alcohol, cigarettes, cocaine, antimetabolites)
     Placental
    • Decreased placental weight, cellularity, or both
    • Decrease in surface area, infarction
    • Villous placentitis (bacterial, viral, parasitic)
    • Tumour (chorioangioma, hydatiform mole)
    • Placental separation
    • Twin to twin transfusion syndrome
     Constitutional
    • Familial and racial background

    Physical examination

    Physical examination should include a detailed search for associated abnormalities:

    • dysmorphic features
      • ‘unusual’ facies
      • abnormal hands and feet
      • abnormal palmar creases
      • in addition to gross anomalies
    • ocular disorders
      • cataracts
      • cloudy cornea
      • chorioretinitis
    • features of intrauterine infection
      • hepatosplenomegaly 
      • jaundice
      • blueberry-muffin rash.

    Problems in SGA

    Problem Pathogenesis
    Intrauterine fetal demise
    • Hypoxia
    • acidosis
    • Infection
    • Lethal anomaly
    Perinatal asphyxia Decreased uteroplacental perfusion in labour +/- chronic fetal hypoxia/acidosis
    Hypoglycaemia
    • Decreased tissue glycogen stores
    • Decreased gluconeogenesis
    • High glucose requirements
    Polycythaemia - hyperviscosity Fetal hypoxia with increased erythropoietin production
    Hypothermia
    • Large surface area
    • Poor subcutaneous fat stores
    Respiratory distress

    Investigations 

    Investigations for SGA include the following:

    • Placental history
    • FBE, platelet count for:
      • suspected sepsis/chronic intrauterine infection
      • unwell baby
      • plethoric baby
    • BGL screen for hypoglycaemia
    • If respiratory distress:
      • ABG
      • chest X-ray.
    • Establish the cause of growth restriction:
      • If intrauterine infection is suspected check maternal TORCH serology and screen infant urine and saliva for CMV (further investigation will be required if suspicion confirmed).
      • If dysmorphic genetic consultation and chromosome studies 
      • If showing signs of withdrawal urine for drug screen.
      • Ultrasonography and echocardiography, if clinically indicated.
      • Opthalmology review

    Management

    At birth

    Hypothermia

    Nurse in a thermoneutral environment.

    Hypoglycaemia

    • Monitor blood glucose.
    • Commence early enteral feeds or intravenous glucose infusion.

    Necrotising enterocolitis (NEC)

    • Infants, particularly preterm SGA, found to have placental insufficiency and abnormal umbilical artery Doppler studies may be at particular risk of developing NEC or gastrointestinal perforation.
    • Enteral feeding should be increased gradually.

    Polycythemia

    Partial volume exchange may be required for symptomatic infants. See polycythemia.

    Outcome

    The outcome for SGA infants is principally determined by the cause.

    Postnatal physical growth

    • Symmetric SGA are smaller and relatively underweight throughout life.
    • Asymmetric SGA accelerated velocity of growth (‘catch up growth‘) in first six months and normal development.

    Neuro-developmental outcome

    • Term SGA no increased risk of severe neurological morbidity compared with term AGA infants. However, increased hyperactivity, short attention span and learning problems may result.
    • Preterm SGA - minor neurological abnormalities are more common than in preterm AGA infants.

    More information

    Clinical

    References

    • Avery GB, Fletcher MA, MacDonald MG, eds. Neonatology. 5th edn. Philadelphia, Pa: Lippincott Williams & Wilkins, 1999:411-444.
    • Rennie JM, Roberton NRC (Eds). Textbook of Neonatology, 3rd edn. Churchill Livingstone , Edinburgh, 1999.
    • Patti J Thureen, Marianne S Anderson and William W. Hay, Jr. Small for gestational age, NeoReviews; 2001; E139-e149.
    • Small for Gestational Age: Causes and Consequences
    • N Engl J Med 2009; 360:2687-2688

    Get in touch

    Centre of Clinical Excellence - Women and Children
    Safer Care Victoria

    Version history

    First published: August 2013

    Last web update: October 2018

    Review by: September 2019

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