In pregnancy, the fetoplacental unit induces major metabolic changes, the purpose of which is to shunt glucose and amino

acids to the fetus while the mother uses ketones and triglycerides to fuel her metabolic needs. These metabolic changes are accompanied by ma- ternal insulin resistance, caused in part by placental production of ster- oids, a growth hormone variant, and placental lactogen. Although pregnancy has been referred to as a state of accelerated starvation, it is better characterized as accelerated ketosis. Pregnancy complicated by diabetes mellitus is associated with higher maternal and perinatal morbidity and mortality rates. Folate supplementation reduces the incidence of fetal neural tube defects, which occur with greater frequency in fetuses of diabetic mothers. Commencing in the third trimester, regular surveillance of maternal glucose control as well as assessment of fetal growth (obstetric sonography) and fetoplacental oxygenation (fetal heart rate monitoring or biophysical profile) optimizes pregnancy outcome. Pregnant diabetic patients without vascular disease are at greater risk for delivering a macrosomic fetus, and attention to fetal growth via clinical and ultrasound examinations is important. Fetal mac- rosomia is associated with an increased risk of maternal and fetal birth trauma. Pregnant women with diabetes have an increased risk of developing preeclampsia, and those with vascular disease are at greater risk for developing intrauterine growth restriction, which is associated with an increased risk of fetal and neonatal death, delivering infants who are large for their gestational age, and birth lacerations. Their fetuses are at risk of hypoglycemia and birth trauma (brachial plexus) injury( most common incidence). All pregnant women should be screened for gestational diabetes unless they are in a low-risk group. Women at low risk for gestational diabe- tes are those <25 years of age; those with a body mass index < 25 kg/ m2 Large for gestational age (LGA) is an indication of high prenatal growth rate, often defined as a weight (or length, or head circumference) that lies above the 90th percentile for that gestational age. Macrosomia, also known as big baby syndrome, is sometimes used synonymously with LGA, or is otherwise defined as a fetus or infant that weighs above 4000 grams (8 lb 13 oz) or 4500 grams (9 lb 15 oz) regardless of gestational age. The pathophysiology of macrosomia is related to the associated maternal or fetal condition that accounts for its development. In general, poorly controlled diabetes, maternal obesity, and excessive maternal weight gain are all associated with macrosomia and have intermittent periods of hyperglycemia in common. Hyperglycemia -> stimulation of insulin, insulinlike growth factors, growth hormone, and other growth factors, which, in turn, stimulate fetal growth and deposition of fat and glycogen.

Fetal macrosomia indicates poor maternal glucose control, and these infants are at risk of stillbirth. Maternal morbidity to be associated with a birth weight of 4500 g or higher postpartum bleeding. Gestational age is associated with macrosomia. Birth weight increases as gestational age increases. Prolonged pregnancies (>41 wk) are associated with an increased incidence of macrosomia. Multiparity and grand multiparity increase the risk of macrosomia A history of macrosomia can influence future pregnancies Fetal sex influences macrosomic potential. (MALE > FEMALE)

Infants born to mothers with glucose intolerance are at an increased risk of morbidity and mortality related to the following: Respiratory distress Growth abnormalities (large for gestational age [LGA], small for gestational age [SGA]) Hyperviscosity secondary to polycythemia Hypoglycemia Congenital malformations Hypocalcemia, hypomagnesemia, and iron abnormalities Metabolic and electrolyte abnormalities Hypoglycemia is caused by hyperinsulinemia due to hyperplasia of fetal pancreatic beta cells consequent to maternal-fetal hyperglycemia. Because the continuous supply of glucose is stopped after birth, the neonate develops hypoglycemia because of insufficient substrate. Hypoglycemia may present within the first few hours of life. Although the infant is generally asymptomatic, symptoms may include jitteriness, irritability, apathy, poor feeding, high-pitched or weak cry, hypotonia, or frank seizure activity. Pulmonary disease These infants are at an increased risk of respiratory distress syndrome and may present within the first few hours after birth with tachypnea, nasal flaring, intercostal retractions, and hypoxia.

Hematologic problems Polycythemia, caused by increased erythropoiesis triggered by chronic fetal hypoxia, may present as a clinically "ruddy" appearance, sluggish capillary refill, or respiratory distress. Hyperviscosity due to polycythemia increases the IDMs risk for stroke, seizure, necrotizing enterocolitis, and renal vein thrombosis. Thrombocytopenia Thrombopoiesis may be inhibited because of an excess of RBC precursors within the bone marrow as a result of chronic in utero hypoxia and increased erythropoietin concentration. Hyperbilirubinemia This is common, especially in association with polycythemia. The increased red cell mass results in increased number of RBCs that are taken out of circulation each day and increase the bilirubin burden presented to the liver. Cardiovascular anomalies Cardiomyopathy with ventricular hypertrophy and outflow tract obstruction may occur in as many as 30% of IDMs. Other abnormalities include: single umbilical artery, VSDs, atrial septal defects, TGA, coarctation of the aorta, cardiomegaly) anomalies are more frequent in these infants. Other organs Renal (eg, hydronephrosis, renal agenesis, ureteral duplication), ear, gastrointestinal (eg, duodenal or anorectal atresia, small left colon syndrome) Determination of plasma or whole blood glucose should be made at the following points: As soon as possible after birth Repeat determinations at 30 minutes, 1 hour, 2 hours, 4 hours, 8 hours, and 12 hours after birth At any time abnormal clinical signs are observed