Infants whose weight is > the 90th percentile for gestational age are classified as large for gestational age (LGA). Macrosomia is birth weight > 4000 g in a term infant. The predominant cause is maternal diabetes. Complications include birth trauma, hypoglycemia, hyperviscosity, and hyperbilirubinemia.
The Fenton growth charts provide a more precise assessment of growth vs gestational age (Fig. 2: Fenton Growth Chart for Preterm Boys and Fig. 3: Fenton Growth Chart for Preterm Girls).
Other than genetically determined size, maternal diabetes mellitus is the major cause of large-for-gestational-age (LGA) infants. The macrosomia results from the anabolic effects of high fetal insulinlevels produced in response to excessive maternal blood glucose during gestation. The less well controlled the mother's diabetes during pregnancy, the more severe is the fetal macrosomia. Rare causes of macrosomia are Beckwith-Wiedemann syndrome (characterized by macrosomia, omphalocele, macroglossia, and hypoglycemia) and Sotos, Marshall, and Weaver syndromes.
Symptoms, Signs, and Treatment
LGA infants are large, obese, and plethoric. The 5-min Apgar score (see Assessment) may be low. These infants may be listless and limp and feed poorly. Delivery complications can occur in any LGA infant. Congenital anomalies and some metabolic and cardiac complications are specific to LGA infants of diabetic mothers.
Because of the infant's large size, vaginal delivery may be difficult and occasionally results in birth injury (see Birth Injuries), particularly including
Therefore, operative delivery (cesarean delivery) should be considered when the fetus is thought to be too large for the pelvis (true cephalopelvic disproportion).
Other complications occur when weight is > 4000 g. There is a proportional increase in morbidity and mortality due to the following:
Infants of diabetic mothers:
Infants of diabetic mothers (IDMs) are at risk of
Hypoglycemia is very likely in the first few hours after delivery because of the state of hyperinsulinism and the sudden termination of maternal glucose when the umbilical cord is cut. Neonatal hypoglycemia can be decreased by close prenatal control of the mother's diabetes and early frequent feedings. Blood glucose levels should be closely monitored by bedside testing from birth through the first 24 h. If there is persistent hypoglycemia, parenteral IV glucose is given.
Hypocalcemia and hypomagnesemia may occur but are usually transient and asymptomatic; serum levels should be checked within the first 72 h after birth. Good prenatal glycemic control decreases the risk of neonatal hypocalcemia. Hypocalcemia typically does not require treatment unless there are clinical signs of hypocalcemia or levels < 7 mg/dL in term infants. Treatment is usually given with IV supplementation of Ca gluconate. Hypomagnesemia can interfere with the secretion of parathyroid hormone, so hypocalcemia may not respond to treatment until the Mg level is corrected.
Polycythemia is slightly more common among IDMs. Elevated insulin levels increase fetal metabolism and thus O2 consumption. If the placenta is unable to meet the increased O2 demand, fetal hypoxemia occurs, triggering an increase in erythropoietin and thus Hct.
Hyperbilirubinemia occurs for several reasons. IDMs have decreased tolerance for oral feedings (particularly when they are preterm) in the earliest days of life, which increases the enterohepatic circulation of bilirubin. Also, if polycythemia is present, the bilirubin load increases.
Respiratory distress syndrome (RDS) may occur because elevated insulin levels decrease surfactant production; pulmonary maturation may thus be delayed until late in gestation. RDS may develop even if the infant is delivered late preterm or term. The lecithin/sphingomyelin ratio, and especially the presence of phosphatidyl glycerol, in amniotic fluid obtained by amniocentesis can evaluate fetal lung maturity and help determine the optimal time for safe delivery. Lung maturity can be assumed only if phosphatidyl glycerol is present. Good prenatal glycemic control decreases the risk of RDS. Treatment is discussed elsewhere (see Treatment). Transient tachypnea of the newborn (see Transient Tachypnea of the Newborn) is 2 to 3 times more likely in IDMs because of the delay in fetal lung fluid clearance.
Congenital anomalies are more likely in IDMs because maternal hyperglycemia at the time of organogenesis is detrimental. Specific anomalies include
Persistently elevated insulin levels can also lead to increased deposition of glycogen and fat into cardiomyocytes. This deposition can cause transient hypertrophic cardiomyopathy, predominantly of the septum.
Last full review/revision January 2015 by James W. Kendig, MD; Ursula Nawab, MD
Content last modified January 2015