We don't know what causes gestational diabetes, but we have some clues. The placenta supports the baby as it grows. Hormones from the placenta help the baby develop. But these hormones also block the action of the mother's insulin in her body. This problem is called insulin resistance. Insulin resistance makes it hard for the mother's body to use insulin. She may need up to three times as much insulin. Show Gestational diabetes starts when your body is not able to make and use all the insulin it needs for pregnancy. Without enough insulin, glucose cannot leave the blood and be changed to energy. Glucose builds up in the blood to high levels, called hyperglycemia. Growing baby, growing impactGestational diabetes affects the mother in late pregnancy, after the baby's body has been formed, but while the baby is busy growing. Because of this, gestational diabetes does not cause the kinds of birth defects sometimes seen in babies whose mothers had diabetes before pregnancy. However, untreated or poorly controlled gestational diabetes can hurt your baby. When you have gestational diabetes, your pancreas works overtime to produce insulin, but the insulin does not lower your blood glucose levels. Although insulin does not cross the placenta, glucose and other nutrients do. So extra blood glucose goes through the placenta, giving the baby high blood glucose levels. This causes the baby's pancreas to make extra insulin to get rid of the blood glucose. Since the baby is getting more energy than it needs to grow and develop, the extra energy is stored as fat. This can lead to macrosomia, or a "fat" baby. Babies with macrosomia face health problems of their own, including damage to their shoulders during birth. Because of the extra insulin made by the baby's pancreas, newborns may have very low blood glucose levels at birth and are also at higher risk for breathing problems. Babies born with excess insulin become children who are at risk for obesity and adults who are at risk for type 2 diabetes. CDC podcastThe Centers for Disease Control and Prevention (CDC) podcast, Gestational Diabetes and Women, tells expectant moms more about diabetes during pregnancy. Learn about managing gestational diabetes, its impact on your future health and what you can do to lower your risk for type 2 diabetes after you've had it.
Communication between members of the perinatal team is of crucial importance to identify infants who are at the highest risk for complications from maternal diabetes. Fetal congenital malformations are most common when maternal glucose control has been poor during the first trimester of pregnancy. As such, the need for preconceptional glycemic control in women with diabetes cannot be overstated. Maternal hyperglycemia during late gestation is more likely to lead to fetal macrosomia, hypoxia, polycythemia, and cardiomegaly with outflow tract obstruction. [1, 2] Fetal macrosomia (>90th percentile for gestational age or >4000 g in the term infant) occurs in 15-45% of diabetic pregnancies. It is most commonly observed as a consequence of maternal hyperglycemia. When macrosomia is present, the infant appears puffy, fat, ruddy, and often hypotonic. [3, 4, 5, 6] Fetal growth is assessed by plotting birth weight against gestational age on standard growth curves. Infants whose weight exceeds the 90th percentile for gestational age are classified as large for gestational age (LGA). Maternal hyperglycemia during late pregnancy is commonly followed by excessive fetal growth. LGA infants should be routinely screened for hypoglycemia. This is particularly important if the mother has received glucose-containing fluids during her labor. Infants whose birthweight is below the 10th percentile, when plotted against gestational age on a standard growth curve, are considered small for gestational age (SGA). Impaired fetal growth may occur in as many as 20% of diabetic pregnancies, compared with a 10% incidence (by definition) for infants born to mothers without diabetes. Maternal renovascular disease is the common cause of impaired fetal growth in pregnancies complicated by maternal diabetes. Perinatal asphyxia, more common in infants with impaired fetal growth, may be anticipated by prenatal history; this demonstrates the importance of communication between the obstetrician and the pediatrician. 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. Operative delivery due to macrosomia also increases the risk for transient tachypnea of the newborn, whereas polycythemia predisposes the infant to persistent pulmonary hypertension of the newborn. Initially, the differential diagnosis includes transient tachypnea of the newborn, respiratory distress syndrome, pneumonia, and persistent pulmonary hypertension. 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. Hypoglycemia that requires intervention may persist for as long as 1 week. 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. Stimulation of fetal insulin release by maternal hyperglycemia during labor significantly increases the risk of early hypoglycemia in these infants. Perinatal stress may have an additive effect on hypoglycemia due to catecholamine release and glycogen depletion. The overall risk of hypoglycemia is anywhere from 25-40%, with LGA and preterm infants at highest risk. Hypocalcemia or hypomagnesemia may also be apparent in the first few hours after birth. Symptoms may include jitteriness or seizure activity. Hypocalcemia (levels < 7 mg/dL) is believed to be associated with a delay in parathyroid hormone synthesis after birth. Sixty-five percent of all infants of diabetic mothers (IDMs) demonstrate abnormalities of iron metabolism at birth. Iron deficiency increases the infant's risk for neurodevelopmental abnormalities. Iron is redistributed to the iron-deficient tissues after birth, as the red blood cell (RBC) mass is postnatally broken down. 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 IDM’s risk for stroke, seizure, necrotizing enterocolitis, and renal vein thrombosis. 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. 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. Cardiomyopathy with ventricular hypertrophy and outflow tract obstruction may occur in as many as 30% of IDMs. [7] The cardiomyopathy may be associated with congestive failure with a weakly functioning myocardium or may be related to a hypertrophic myocardium with significant septal hypertrophy and outflow tract obstruction. When cardiomegaly or poor perfusion and hypotension are present, performing echocardiography to differentiate between these processes is important. These infants are also at an increased risk of congenital heart defects, including (most commonly) ventricular septal defect (VSD) and transposition of the great arteries (TGA). Central nervous system (CNS) malformations are 16 times more likely in IDMs. In particular, the risk of anencephaly is 13 times higher, whereas the risk of spina bifida is 20 times higher. The risk of caudal dysplasia is up to 600 times higher in these infants. [8] Neurologic immaturity, demonstrated by immature sucking patterns, has been found in infants born to insulin-managed mothers with diabetes. [9] Studies in fetal sheep indicate that this may be a reflection of the abnormal brain metabolism and electroencephalogram (EEG) findings as a result of the fetal hyperglycemia. [10] Renal (eg, hydronephrosis, renal agenesis, ureteral duplication), ear, gastrointestinal (eg, duodenal or anorectal atresia, small left colon syndrome), and, as mentioned earlier, cardiovascular (eg, single umbilical artery, VSDs, atrial septal defects, TGA, coarctation of the aorta, cardiomegaly) anomalies are more frequent in these infants.
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. Poor maternal glycaemic control during embryogenesis can result in a four- to eight-fold increase in congenital malformations including:
However, these are not seen with an increased frequency in infants of diabetic fathers, or mothers where gestational diabetes develops after the first trimester. Perinatal complications of diabetes in pregnancyPerinatal complications include Increased perinatal mortality due to: Birth injury may be caused by:
Neonatal complications of diabetes in pregnancyNeonatal complications include:
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What is the newborn of a diabetic mother at risk to develop?
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