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Skip navigation A service of the U.S. National Library of Medicine National Institutes of Health Home About MedlinePlus Site Map FAQs Contact Us Search MedlinePlus Health Topics Drugs & Supplements Videos & Cool Tools ESPAÑOL Infant of diabetic mother Share on facebook Share on twitter Bookmark & Share Printer-friendly version An infant of a diabetic mother is a baby who is born to a mother with diabetes. The baby's mother had high blood sugar (glucose) levels throughout her pregnancy. Causes High blood sugar level in a pregnant woman can affect the infant after birth. Infants who are born to mothers with diabetes are often larger than other babies. Organs such as the liver, adrenal glands, and heart are likely to be enlarged. These infants may have periods of low blood sugar (hypoglycemia) shortly after birth because of increased insulin level in their blood. Insulin is a substance that moves sugar (glucose) from the blood into body tissues. The infant's blood sugar level will need to be closely monitored in the first 12 to 24 hours of life. Mothers with poorly controlled diabetes are also more likely to have a miscarriage or stillborn child. The delivery may be difficult if the baby is large. This can increase the risk for brachial plexus injuries and other trauma during birth.

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HYPERLINK "http://www.nlm.nih.gov/medlineplus/ency/article/001597.htm" \o "Printer-friendly version" Printer-friendly versionAn infant of a diabetic mother is a baby who is born to a mother with diabetes. The baby's mother had high blood sugar (glucose) levels throughout her pregnancy.

Causes

High blood sugar level in a pregnant woman can affect the infant after birth.

Infants who are born to mothers with diabetes are often larger than other babies. Organs such as the liver, adrenal glands, and heart are likely to be enlarged.

These infants may have periods of low blood sugar (hypoglycemia) shortly after birth because of increased insulin level in their blood. Insulin is a substance that moves sugar (glucose) from the blood into body tissues. The infant's blood sugar level will need to be closely monitored in the first 12 to 24 hours of life.

Mothers with poorly controlled diabetes are also more likely to have a miscarriage orstillbornchild. The delivery may be difficult if the baby is large. This can increase the risk for brachial plexus injuries and other trauma during birth.

If the mother had diabetes before her pregnancy, her infant has an increased risk of birth defects if the disease was not well controlled.

Symptoms

The infant is oftenlarge for gestational age. Other symptoms may include:

Blue or patchy (mottled) skin color, rapid heart rate, rapid breathing (signs of immature lungs or heart failure)

Newborn jaundice(yellow skin)

Poor feeding, lethargy, weak cry (signs of severe low blood sugar)

Puffy face

Reddish appearance

Tremors or shaking shortly after birth

Exams and Tests

Before the baby is born:

Ultrasound performed on the mother in the last few months of pregnancy to assess the babys development will show that the baby is large for gestational age.

Lung maturity testing may be done on the amniotic fluid if the baby is going to be delivered more than a week before the due date.

After the baby is born:

Tests may show that the infant has low blood sugar and low blood calcium.

An echocardiogram may show an abnormally large heart, which can occur with heart failure.

Treatment

All infants who are born to mothers with diabetes should be tested for low blood sugar (hypoglycemia), even if they have no symptoms.

If an infant had one episode of low blood sugar, tests to check blood sugar level will be done over several days. Testing will be continued until the infant's blood sugar remains stable with normal feedings.

Feeding soon after birth may prevent low blood sugar in mild cases. Low blood sugar that does not go away is treated with sugar (glucose) and water given through a vein.

Rarely, the infant may need breathing support or medicines to treat other effects of diabetes. High bilirubin levels are treated with light therapy (phototherapy). Rarely, the baby's blood will be replaced with blood from a donor (exchange transfusion) for this problem.

Outlook (Prognosis)

Often, an infant's symptoms go away within a few weeks. However, an enlarged heart may take several months to get better.

Possible Complications

Congenital heart defects

Heart failure

High bilirubin level (hyperbilirubinemia) -- may cause permanent brain damage if it is not treated

Immature lungs

Neonatal polycythemia(more red blood cells than normal) -- this may cause a blockage in the blood vessels or hyperbilirubinemia

Severe low blood sugar - may cause permanent brain damage

Small left colon syndrome - causes symptoms of intestinal blockage

Stillbirth

When to Contact a Medical Professional

If you are pregnant and receiving regular prenatal care, routine testing will show if you develop gestational diabetes.

If you are pregnant and have diabetes that is not under control, call your doctor right away.

If you are pregnant and are not receiving prenatal care, call your health care provider for an appointment. You can also call the State Board of Health for instructions on how to obtain state-assisted prenatal care.

Prevention

Women with diabetes need special care during pregnancy to prevent complications. Controlling blood sugar and getting diagnosed with gestational diabetes early can prevent many problems.

Lung maturity testing may help prevent breathing complications that can occur if the baby is being delivered more than a week before the due date.

Carefully monitoring the infant in the first hours after birth may prevent complications due to low blood sugar. Monitoring and treatment in the first few days may prevent complications due to high bilirubin level.

Alternative Names

IDM

Update Date: 12/4/2013

Updated by: Neil K. Kaneshiro, MD, MHA, Clinical Assistant Professor of Pediatrics, University of Washington School of Medicine, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Bethanne Black, and the A.D.A.M. Editorial team.

Browse the EncyclopediaMedlinePlus Topics Diabetes and PregnancyRead More Blood sugar test - blood Diabetes

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Infant of Diabetic Mother

Updated: May 10, 2013

Overview Complications Workup Hypoglycemic Management Transfer, Consultations, and Follow-Up Show AllMultimedia LibraryReferencesOverview

Infants of diabetic mothers (IDMs) have experienced a nearly 30-fold decrease in morbidity and mortality rates since the development of specialized maternal, fetal, and neonatal care for women with diabetes and their offspring. Before then, fetal and neonatal mortality rates were as high as 65%.

Today, 3-10% of pregnancies are affected by abnormal glucose regulation and control. Of these cases, 80-88% are related to abnormal glucose control of pregnancy or gestational diabetes mellitus. Of mothers with preexisting diabetes, 35% have been found to have type 1 diabetes mellitus, and 65% have been found to have type 2 diabetes mellitus.

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

These infants are likely to be born by cesarean delivery for many reasons, among which are such complications as shoulder dystocia with potential brachial plexus injury related to the infant's large size. These mothers must be closely monitored throughout pregnancy. If optimal care is provided, the perinatal mortality rate, excluding congenital malformations, is nearly equivalent to that observed in normal pregnancies.

Complications

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

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]Fetal growth is assessed by plotting birth weight againstgestational ageon 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 forhypoglycemia. This is particularly important if the mother has received glucose-containing fluids during her labor.

Impaired fetal growth

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.

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. 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 includestransient tachypneaof the newborn, respiratory distress syndrome,pneumonia, and persistent pulmonary hypertension.

Metabolic and electrolyte abnormalities

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.

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. 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)andtransposition of the great arteries (TGA).

Congenital malformations

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.[6]Neurologic immaturity, demonstrated by immature sucking patterns, has been found in infants born to insulin-managed mothers with diabetes.[7]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.[8]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.

Workup

CBC count

Polycythemia, commonly defined as a centralhematocritlevel higher than 65%, is a potential concern. Maternal-fetal hyperglycemia and fetal hypoxia is a strong stimulus for fetalerythropoietinproduction and subsequent increase in fetalhemoglobin concentration. Thrombocytopenia may occur because of impaired thrombopoiesis due to "crowding-out" of thrombocytes by the excess of erythroid precursors in the bone marrow.

Glucose concentration (serum or whole-blood)

Seizures, coma, and long-term brain damage may occur if neonatal hypoglycemia is unrecognized and untreated. Most centers recognize levels lower than 20-40 mg/dL within the first 24 hours after birth as abnormal, but the precise level remains controversial.[9]A policy to screen infants of diabetic mothers (IDMs) for hypoglycemia should be in place in every hospital. Operational thresholds were proposed by Cornblath et al.[10]They suggested that an infant with compromised metabolic adaptation (ie, IDM) undergo bloodglucosemeasurements (1) as soon as possible after birth, (2) within 2-3 hours after birth and before feeding, and (3) at any time abnormal clinical signs are observed.

Magnesium concentration (serum)

Hypomagnesemia is related to younger maternal age, severity of maternal diabetes, and prematurity. Neonatalmagnesiumlevels are also related to maternal serum magnesium, neonatal calcium andphosphoruslevels, and neonatal parathyroid function. The clinical significance of low magnesium levels in these infants remains controversial and uncertain.

Calcium concentration (serum, ionized or total levels)

Lowserum calciumlevels in IDMs are common. They are speculated to be caused by a functional hypoparathyroidism; however, their clinical relevance remains uncertain and controversial.

Bilirubin level (serum, total and unconjugated)

Hyperbilirubinemia (seebilirubin) is notably more common in IDMs than in the general population of neonates. Causative factors include prematurity, hepatic enzyme immaturity, polycythemia, and reduced RBC half-life.

Arterial blood gas

Assessing oxygenation and ventilation is essential in infants with clinical evidence of respiratory distress. Although noninvasive methods (eg, transcutaneous oxygen and carbon dioxide electrodes, oximeters) have gained wide acceptance at many centers, comparison of results with those from arterial blood is intermittently required.

Chest radiography

Clinical evidence of cardiopulmonary distress requires a detailed evaluation, which should always include a chest radiograph. The image should be evaluated for adequacy of lung expansion, evidence of focal or diffuse atelectasis, presence of interstitial fluid, signs of free air in pleural or interstitial spaces, and findings of respiratory distress syndrome or pneumonia. The possibility of pulmonary malformations should also be considered.

Cardiac size, shape, and great vessel/outflow tract should be carefully examined. In the infant with macrosomia who has a history of shoulder dystocia, the clavicles should be evaluated on the film as well on physical examination.

Abdominal, pelvic, or lower extremity radiography

When caudal dysplasia is present, other orthopedic anomalies should be investigated, including fusion of the legs, hypoplastic femur, defects of the tibia and the fibula, flexion contractures of the knee and hip, or clubfoot. Caudal dysplasia or sacral agenesis is the most common orthopedic anomaly in the IDM.

Lower extremity congenital malformations require radiographic evaluation to determine the exact skeletal defect or defects present.

Cardiac echocardiography

A thickened myocardium and significant septal hypertrophy may be present in as many as 1 in 3 IDMs. Evidence of a hypercontractile, thickened myocardium, often with septal hypertrophy disproportionate to the size of the ventricular free walls, may be noted on examination. Myocardial contractility should also be evaluated, because the myocardium is overstretched and poorly contractile with congenital cardiomyopathies.

Evidence of anatomical malformation must be searched for carefully because cardiac malformations, including VSDs and TGAs, are significantly more common in IDMs.

Barium enema

Infants with feeding intolerance, abdominal distention, nonbilious emesis, or poor passage of meconium may require a barium enema. Congenital anomalies of the gastrointestinal tract are more common in IDMs. These infants may have small left colon syndrome, also known as "lazy colon."

Clinical features of the small left colon syndrome may mimic those of Hirschsprung disease, and distal tapering of the colon is a radiologic feature of both disorders. The 2 disorders can be distinguished using a biopsy because normal ganglionic cells are present in lazy colon and absent inHirschsprung disease.

Indwelling vascular lines (peripheral, umbilical, or central)

Noninvasive blood gas monitoring using transcutaneous electrodes (PaO2and PaCO2) and oximeters (O2% saturation) has greatly reduced the need for invasive, indwelling catheters. However, indwelling lines are often needed early in the course of cardiorespiratory disease. In some instances, the need for continuous arterial blood pressure monitoring may warrant placement of a peripheral or umbilical arterial line.

Placement of an umbilical venous or a central venous catheter is often used when the infant requires high concentrations of intravenous (IV) dextrose or when peripheral access is limited or exhausted.

Histologic findings

The pancreas has larger and more numerous islets (see image below). Sections from neonatal myocardium show cellular hyperplasia and hypertrophy.

An increase in the number and size of the islets is commonly seen in the pancreas of infants born to diabetic mothers.Hypoglycemic Management

Improved maternal glucose control during the pregnancy and labor improves postnatal glucose adaptation and a decreases the need for IV glucose treatment in the infant. A screening policy for hypoglycemia during the hours after birth is necessary to detect hypoglycemia.

Serum or whole blood glucose levels of less than 20-40 mg/dL within the first 24 hours after birth are generally agreed to be abnormal and to require intervention. Cornblath et al recommended critical values of glucose that require intervention.[10]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

Guidelines for maintaining euglycemia

If the plasma value is less than 36 mg/dL (2 mmol/L), intervention is needed (1) if plasma glucose remains below this level, (2) if it does not increase after a feeding, or (3) if the infant develops symptoms of hypoglycemia.

If the plasma value is less than 20-25 mg/dL (1.1-1.4 mmol/L), IV glucose should be administered, with the target glucose level being more than 45 mg/dL (2.5 mmol/L). This goal of 45 mg/dL is accentuated as a margin of safety. This should include a bolus of dextrose followed by a constant infusion of dextrose. Profound hypoglycemia may require therapy with hydrocortisone.

Determining which infants require the highest dextrose administration to maintain euglycemia is difficult. The following suggestions represent a guideline for glucose administration to an infant with hypoglycemia.

Immediate IV therapy with 2-mL/kg infusion of dextrose 10% is required in any symptomatic infant with hypoglycemia; dextrose 10% (D10) provides 100 mg/mL of dextrose, and the starting dose is 200 mg/kg of dextrose. Administration over 5-10 minutes is usually recommended because of the high osmolarity. This is especially true for immature infants younger than 32 weeks' gestational age who are at some risk for intracranial hemorrhage. This procedure originally was described as a 2-minute infusion and accomplishes a filling of the glucose space analogous to the volume of distribution of glucose.

Maintenance of a continuous infusion of dextrose at an infusion rate of 6-8 mg/kg/min of dextrose is necessary once bolus therapy is complete. Failure to do so may result in rebound hypoglycemia as a result of heightened pancreatic insulin release triggered by the glucose infusion.

Frequent serum or whole blood glucose analyses are important to properly titrate the dextrose infusion. Should follow-up glucose levels remain less than 40 mg/dL, the dextrose infusion may be increased by 2 mg/kg/min until euglycemia is achieved.

If the infant requires a dextrose concentration of more than D12.5 through a peripheral vein at 80-100 mL/kg/day, placement of a central venous catheter may be considered to avoid venous sclerosis. Continued enteral feedings hasten improvement in glucose control because of the presence of protein and fat in the formula. Hydrocortisone therapy may be required for ongoing hypoglycemia.

Once the infant's glucose levels have been stable for 12 hours, IV glucose may be tapered by 1-2 mg/kg/min, depending on maintenance of preprandial glucose levels higher than 40 mg/dL.

Electrolyte management

Hypocalcemia and hypomagnesemia may complicate the clinical course. Because low serum calcium levels cannot be corrected in the presence of hypomagnesemia, correction of low magnesium levels is an initial step in the treatment of hypocalcemia.

In infants of diabetic mothers (IDMs), calcium and magnesium levels are commonly measured within the first hours after birth. Ideally, ionized levels of these electrolytes should be obtained and used to properly manage these electrolyte disturbances.

True symptomatic hypocalcemia is extremely rare in these infants. In most cases, symptoms interpreted to be caused by low calcium or magnesium levels are due to low glucose levels associated with perinatal asphyxia or associated with various CNS problems.

Low levels may be treated by adding calcium gluconate to the IV solution to deliver 600-800 mg/kg/day of calcium gluconate. Bolus therapy should be avoided unless cardiac arrhythmia is present. Bolus therapy may result in bradycardia.

Respiratory management

Pulmonary management is tailored to the individual infant's signs and symptoms. Increased ambient oxygen concentrations may be required to maintain oxygen saturations higher than 90%, transcutaneous oxygen tensions at 40-70 mm Hg, or arterial oxygen tensions at 50-90 mm Hg.

When an inspired oxygen concentration (FiO2) higher than 40% is required, the most important task is to determine a precise diagnosis of the cause for the hypoxemia and to administer therapy appropriate for the underlying pathophysiology.

Assisted ventilation

Nasal continuous positive airway pressure (NCPAP) or endotracheal intubation with intermittent mandatory ventilation (IMV) or synchronized positive pressure ventilation (SIMV) may be used for the management of severe respiratory distress.

Common criteria for such interventions include inspired oxygen requirements (FiO2) of 60-100% to maintain arterial PO2of 50-80mm Hg, arterial PCO2levels higher than 60 mm Hg or rising 10 mm Hg, and apnea. The specific criteria for using these modes of assisted ventilation may vary depending on the underlying respiratory pathology and clinical condition of the infant.

Cardiac management

If signs of congestiveheart failureor cardiomyopathy with cardiomegaly, hypotension, or significant cardiac murmur are observed, echocardiographic evaluation is essential to distinguish among cardiac anomalies, septal hypertrophy, and/or cardiomyopathy.

Once a precise diagnosis is available, management of the cardiac disorder is no different for the IDM than for any other newborn with a similar cardiac condition. Extreme care in the use of cardiotonic agents is important in the presence of any hypertrophic cardiomyopathy or significant septal hypertrophy. These infants are at risk for actual decreased left ventricular output resulting from this form of therapy. Beta blockers, such as propranolol, may be used to relieve the outflow obstruction that is seen with septal hypertrophy.

Transfer, Consultations, and Follow-Up

Infants of diabetic mothers (IDMs) having congenital anomalies, heart disease, or significant respiratory illness may require transfer to a tertiary care neonatal intensive care unit (NICU) for continued care and access to subspecialists. Because of the frequency with which cardiac problems occur in IDMs, early consultation with a pediatric cardiologist often is necessary. Other consultations depend on which other congenital malformations or complications are present.

Basic outpatient care should consist of routine well-baby care provided by the infant's general pediatrician. Additional follow-up by consultant subspecialists depends on the neonatal clinical problems and their resolution..

Why are the classifications important?

The classification of diabetes during pregnancy is important because the outcome of both the mother and the baby are related to the severity and the duration (represented by the different classes) of the mother's diabetic condition.

In mothers withgestational diabetes, there is an increased risk of large (macrosomic) babies and babies with low blood sugars (hypoglycemia) after birth; however, the overall risk of complications is low.

Large babies and babies with low blood sugars also are associated withClasses A, B, C, and D.1Large (macrosomic) babies increase the need for cesarean section delivery because the baby can be too big to pass through the mother's pelvis and vaginal canal.

Class Fmothers have the highest risk of delivering abnormally small babies with poor growth while inside the mother's uterus.1 Class F mothers also have an increased risk of anemia, high blood pressure (hypertension), and decreased kidney function.

Class Hmothers have an increased risk of a heart attack or heart failure and sudden death, along with an increased risk of producing abnormally small babies.

Class Rmothers have an increased risk of worsened retinopathy, bleeding into the eye (vitreous hemorrhage), or detachment of the retina. They also have an increased risk of delivering small babies, most often by cesarean section.

All classeshave an increased risk of abnormally large amounts of amniotic fluid (polyhydramnios). Polyhydramnios increases the risk of pre-term labor and delivery, delivery of the baby's umbilical cord before the baby (cord prolapse), or early separation of the placenta from the uterus (placental abruption). Cord prolapse and placental abruption can dangerously cut off blood supply to the placenta and the baby.

- See more at: http://www.advancedpediatricassociates.com/pediatrichealthlibrary/infantofadiabeticmother.asp#sthash.mXOgmGYE.dpuf_1491436548.unknown

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