Infant of a Diabetic Mother
The classifications of maternal diabetes are outlined in Table 1.
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
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
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.
Infants of diabetic mothers, or IDMs, have a significantly increased risk of breathing
problems (respiratory distress), especially if they are born before
37 weeks, because their lungs are slower to mature.
Approximately 30% to 40% of IDMs have low blood sugar (i.e., glucose
is less than 40 mg/dl) after birth. This condition usually occurs early after birth,
often by one to two hours of age. Low blood sugar occurs because of excess insulin
in the baby. The excess insulin was produced in the baby while inside the mother’s
uterus in response to high blood sugars delivered across the placenta from the mother’s
blood. Prolonged or severe low blood sugar (i.e., hypoglycemia) can cause seizures
and brain damage. Therefore, IDMs will have their blood sugars checked (usually
by “heel stick”) shortly after birth and then several times over the next one to
Approximately 20% of IDMs will have low calcium. If a baby is very
sick, shaky, or lethargic, or has seizures despite normal blood glucose, a blood
calcium measurement should be performed.
An abnormally high red blood cell count (polycythemia) can occur in
IDMs, increasing their risk of jaundice (yellow skin color), feeding
difficulties, respiratory distress, or lethargy. The risk of jaundice is increased
significantly in IDMs even if they are not polycythemic. One study found that 19%
of IDMs developed bilirubin levels greater than 16 mg/dl. Bilirubin is the yellow
pigment that comes from the red blood cells and produces the yellow skin color.
When there is too much bilirubin in a baby’s blood, it can cause brain damage. Fortunately,
this problem is treated easily with light treatment (phototherapy).
The incidence of major congenital anomalies (birth defects) is increased
from 6% to 9% in IDMs, compared to a rate of 2% in the general population. The frequency
of congenital anomalies is not increased in gestational diabetes; however, two-thirds
of these anomalies involve the brain, the nervous system, or the heart. Caudal agenesis
(failure of formation of the lower vertebrae and sacrum of the spine) more frequently
occurs in IDMs whose mothers had poor blood sugar control around the time of conception
and during the first few weeks of pregnancy.
A significant decrease in the incidence of congenital anomalies has been reported
with rigorous glucose control in the periconception period.2 Congenital anomalies
can be reduced even more if the mother takes folate supplements during the early
part of pregnancy.
Poor feeding is a common problem that affects up to 37% of IDMs, often
prolonging the hospital stay.
Macrosomia (large birth weight, i.e., larger than 4 kilograms, or
8 pounds) occurs in about one-third of IDMs, and it correlates with high blood sugars
and serum fat concentrations in the third trimester of pregnancy.3 Usually, macrosomia
is not seen in those mothers with more severe and longer-standing diabetes (e.g.,
Classes F and R).
Poor heart function or myocardial dysfunction is rare, but increased,
in IDMs because of the enlargement of the septum or the wall between the ventricles
(the two large pumping chambers of the heart). This condition is called ventricular
septal hypertrophy, and can cause congestive heart failure, poor cardiac output,
and heart enlargement. However, it often has no associated problems. Sometimes,
a heart murmur is heard when IDMs have poor heart function.
Even when there are associated problems with the heart, they usually resolve by
two weeks, and the hypertrophy resolves by four months. Good diabetic control during
pregnancy can reduce the incidence and the severity of this complication.
Renal vein thrombosis or clotting of the vessel draining blood from
the kidney, causing the kidney to swell, is rare; however, it can occur before or
after birth in IDMs. It is caused by abnormally low blood anticoagulants that may
develop in the baby whose mother is poorly controlled for her diabetes during pregnancy.
Small left colon syndrome can occur in IDMs. This syndrome can cause
the delayed passage of a stool after birth, resulting in abdominal distention and
a delay in normal feeding.
Good glucose control and prevention of ketoacidosis prior to conception
and in the first two months of pregnancy will decrease the risk of congenital anomalies.
Later in the pregnancy, glucose control is important to prevent macrosomia, hypoglycemia
(after birth), and ventricular septal hypertrophy of the baby’s heart. It generally
is recommended that the mother’s fasting blood glucose should be from 70 to 90 mg/dl,
and, two hours after eating, her blood glucose should be less than 120 mg/dl.2
If a pregnant diabetic woman participates in a program of pregnancy management
and surveillance from before conception until delivery, she has at least a 95% chance
of having a completely healthy child.1
Early screening for congenital anomalies usually includes a serum alpha-fetoprotein
level of the mother to screen for open neural tube defects (spina bifida)
and a detailed ultrasound at 18 to 20 weeks. Follow-up ultrasounds
may be required for polyhydramnios (increased amniotic fluid), abnormal fetal growth,
or early separation of the placenta.
Tests of fetal well being, including daily fetal movement counts
and biweekly biophysical testing (ultrasound and fetal heart rate monitoring),
usually begin at 28 to 32 weeks.
An amniocentesis may be performed prior to delivery if the mother is at less than
38 weeks gestation to document fetal lung maturity.
The mother’s glucose will be monitored closely during labor, and insulin and glucose
treatments often will be adjusted.
The baby will require frequent blood glucose checks after birth, beginning
in the first two hours of birth. These check-ups usually are continued every 2 to
4 hours for at least 24 hours.
The red blood cell count, or hematocrit, will be checked after birth
to ensure that the baby does not have polycythemia. If significant jaundice occurs,
bilirubin levels will be checked.
If the baby has jitteriness, lethargy, or poor feeding, despite normal glucoses,
the calcium level will be checked.
A thorough physical examination will be performed to look for any
physical abnormalities and to listen to the heart for any evidence of a heart murmur.
The baby’s long-term development will be followed; studies have shown a mild decrease
in IQs (93 versus 102) of IDMs with a maternal history of ketones in the urine (ketonuria)
during pregnancy, as compared to IDMs with no maternal ketonuria.2 However, significant
differences in mental development have not been found between IDMs with good sugar
control without ketonuria and other normal babies.
If the baby is well after birth, he/she should be
nursed or given formula in the first hour. The first blood sugar should
be checked within two hours of birth or sooner if the baby develops jitteriness,
lethargy, or seizures. If the blood sugar is low (less than 40 mg/dl), the baby
should be fed immediately, and the blood sugar rechecked within one to two hours.
If the blood sugar is extremely low (less than 25 mg/dl), if the baby is sick or
unable to eat, or if the blood sugar remains low despite feeding, an IV
with glucose water should be started for the baby. The blood sugar will be rechecked
frequently until it is normal and stable.
If congenital anomalies exist, they will need to be treated accordingly; some birth
defects may require surgery.
If the baby develops significant jaundice, phototherapy may be required
for a short period (usually from two to five days) to break down the bilirubin in
If the lungs are not mature, the baby could require help with breathing using a
machine called a respirator. The baby also could benefit from surfactant.
Surfactant is a soap suds-like material that is administered to help lubricate and
expand the lungs. Surfactant often is deficient in immature lungs, and most commonly
occurs in those IDMs born at less than 37 weeks.
If the baby has difficulty feeding, he/she may require intermittent gavage feeds
with a feeding tube. Extra time in the hospital may be required for
the baby to learn to feed by either the breast or the bottle.
If the baby develops abdominal distention or has difficulty stooling, a gastrointestinal
x-ray with gastrograffin may be required to check if a microcolon is
In a series of studies from the Joslin Diabetes Center, only 2% to 3%
of IDMs developed insulin-dependant diabetes mellitus before 20 years of age. The
risk of subsequent diabetes is slightly higher if both the mother and the father
have insulin-dependent diabetes. The risks and the complications to the baby outlined
herein do not pertain when only the father has insulin-dependant diabetes.
Cloherty JP, Stark AR. Manual of neonatal care. Philadelphia, Lippencott-Raven,
Fanaroff AA, Martin RJ. Metabolic and endocrine disorders. In: Neonatal-perinatal
medicine: diseases of the fetus and infant. 6th ed. St. Louis: Mosby-Year Book,
About the Author
Dr. Paisley is a second year fellow in Neonatal-Perinatal Medicine in the Section
of Neonatology, Department of Pediatrics, University of Colorado School of Medicine
in Denver, Colorado. Jan trained in Pediatrics at the University of Utah and was
honored to receive a highly prestigious Pediatric Scientist Development Program
Jan preferred clinical practice, however, and she has been working for the past
7 years as a general Pediatrician in Ft. Collins, Colorado.
She joined the Neonatal-Perinatal Medicine Training Program in 1998 and is working
with Dr. Adam Rosenberg and Dr. William Hay on aspects of cerebral glucose metabolism
in a fetal animal model and in newborn human infants.
Dr. Hay is a Professor of Pediatrics at the University of Colorado School of Medicine,
He is the Director of the Training Program in Neonatal-Perinatal Medicine, Director
of the Neonatal Clinical Research Center (as Associate Director of the National
Institutes of Health and Department of Pediatrics sponsored Pediatric Clinical Research
Center), and Scientific Director of The Perinatal Research Center at the University
of Colorado Health Sciences Center.
Dr. Hay holds three NIH research grants and a NIH Training Grant in Perinatal Medicine
His clinical and basic research interests focus on fetal physiology, fetal and neonatal
nutrition and metabolism, glucose disorders in preterm infants, small-for-gestational
aged infants, and infants of diabetic mothers, and oxygen monitoring.
Dr. Hay is Secretary-Treasurer of the American Pediatric Society and is a member
of the NIH Human Embryology and Development Study Section. He travels widely around
the United States and internationally as a visiting scientist and professor.
Dr. Hay also is the senior editor for Current Pediatric Diagnosis and Treatment
(a Lange Publication) and co-editor of NeoReviews (American Academy
Copyright 2012 Jan E. Paisley, M.D., All Rights Reserved
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