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Infant of diabetic mother

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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.
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 often large 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 Encyclopedia

MedlinePlus Topics
Diabetes and Pregnancy

Read 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 All

Multimedia Library
References

Overview
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 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.

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 includes transient tachypnea of 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) and transposition 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 central hematocrit level higher than
65%, is a potential concern. Maternal-fetal hyperglycemia and fetal
hypoxia is a strong stimulus for fetal erythropoietin production 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 blood glucose measurements (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. Neonatal magnesium levels are also related to
maternal serum magnesium, neonatal calcium and phosphorus levels, 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)

Low serum calcium levels 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 (see bilirubin) 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 in Hirschsprung disease.

Indwelling vascular lines (peripheral, umbilical, or central)

Noninvasive blood gas monitoring using transcutaneous electrodes
(PaO and PaCO ) and oximeters (O % 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.
2

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 (FiO ) 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.
2

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 (FiO ) of 60-100% to maintain arterial PO of 50-80mm Hg,
arterial PCO levels 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.
2

Cardiac management
If signs of congestive heart failure or 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 with gestational 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 with Classes A, B, C,
and D.1 Large (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 F mothers 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 H mothers 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 R mothers 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 classes have 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.
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