You are called to the nursery by the postpartum nurse to evaluate a 3-hour-old female infant with tachypnea

You are called to the nursery by the postpartum nurse to evaluate a 3-hour-old
female infant with tachypnea. She was born at 36 weeks of gestation to a 38-yearold woman whose pregnancy was complicated by type 2 diabetes, initially treated
with metformin but due to inadequate glycemic control, insulin was added during
the second trimester. The mother was noncompliant with blood glucose monitoring and insulin therapy, and her hemoglobin A1C at delivery was 12%. Labor
began spontaneously and rupture of membranes occurred 2 hours before delivery. The infant is on the warmer, weighs 4200 g, has a pulse of 140 beats/min, and
respirations of 72 breaths/min with intercostal retractions and nasal flaring. She is
jittery and plethoric. A capillary glucose measured with the bedside glucometer
is 30 mg/dL.
» What is the next step in the evaluation of this infant?
» What is the treatment for this infant?
» What are other possible causes of this infant’s tachypnea?
Summary: A macrosomic neonate is born to a diabetic mother with poor glucose
control. The infant has symptomatic hypoglycemia, a medical emergency.
š Next step: Send a stat serum glucose to confirm the presence of hypoglycemia.
Bedside glucometers measure the glucose in whole blood and tend to be 10%
lower than serum values. The range of difference is greater at lower glucose
š Treatment: Administer intravenous (IV) glucose.
š Other causes of tachypnea in the IDM: Respiratory distress syndrome (RDS)
hypertrophic cardiomyopathy, hypocalcemia, polycythemia, and clavicle fracture.

  1. Recognize the clinical features that may occur in the IDM (Figure 2–1).
  2. Know the management of complications occurring in the IDM, the most common of which is neonatal hypoglycemia.
    Maternal hyperglycemia very early in gestation can cause significant birth defects,
    including neural tube defects and congenital heart disease. Later, in response to
    poorly controlled maternal hyperglycemia, fetal hyperinsulinism begins in the second trimester resulting in fetal macrosomia and increased fetal oxygen requirements.
    Fetal insulin production causes increased glycogen production which is
    deposited in the fetal liver, heart, kidneys, and skeletal muscle. The large shoulders and abdomen of such infants make delivery difficult and the infant may sustain shoulder dystocia, clavicle fracture, or brachial plexus injury. Hypertrophic
    cardiomyopathy results from glycogen deposition in the myocardium. Increased
    fetal oxygen requirements cause polycythemia. Insulin appears to interfere with
    cortisol’s ability to induce surfactant production, which predisposes the neonate
    to RDS. After delivery and removal from the high-sugar in utero environment,
    the infant’s hyperinsulinism can cause hypoglycemia, which must be managed
    immediately. If the hypoglycemia is left untreated, seizures, obtundation, and
    respiratory arrest can occur.
    GESTATIONAL DIABETES MELLITUS (GDM): Persistent hyperglycemia during pregnancy, with serum glucose levels greater than 95 mg/dL in the fasting state
    and above the thresholds for the oral glucose tolerance test.
    HYPOGLYCEMIA: A blood glucose level less than 40 mg/dL is the usual definition, although other definitions exist. Symptoms include lethargy, listlessness, poor
    feeding, temperature instability, apnea, cyanosis, jitteriness, tremors, seizure activity, and respiratory distress.
    MACROSOMIA: Larger than normal baby with the birth weight exceeding the
    90th percentile for gestational age, or any birth weight more than 4 kg.
    Diabetes affects an average of 7% of pregnancies. For most women, the condition
    is transient, occurring during pregnancy and disappearing after delivery. Women
    are screened for gestational diabetes between 24 and 28 weeks of pregnancy (but can
    be screened earlier if considered high risk). If hyperglycemia is present in the first
    trimester, an increased risk for congenital anomalies of the central nervous system,
    heart, kidneys, and the skeletal system (such as caudal regression syndrome in
    which there is hypoplasia of the sacrum and lower extremities) is noted. Women
    who require insulin therapy are at higher risk for a poor perinatal outcome as compared to those whose carbohydrate intolerance can be managed by diet alone. The
    better the glycemic control, the lower the rates of malformations, macrosomia, and
    Hypoglycemia develops in about 25% to 50% of infants born to mothers with
    pregestational diabetes and in about 25% of infants born to mothers with gestational diabetes. Therefore, all IDM should feed within the first hour of life and have
    a bedside glucose measurement approximately 30 minutes after the feed. A blood
    glucose level of less than 40 mg/dL with any symptom of hypoglycemia requires IV
    glucose. If no symptoms of hypoglycemia are present, the infant is refed and the glucose is remeasured 30 minutes after the feeding. Glucose levels in the first 4 hours
    of life that do not increase above 25 mg/dL despite feeding will also require
    IV glucose. Monitoring of glucose typically continues for the first 12 hours of life
    and until three consecutive preprandial measurements are normal. Feeding patterns are monitored closely as poor feeding in the IDM can represent a metabolic
    or cardiac abnormality. Hypocalcemia is another metabolic abnormality commonly
    seen in IDM and presents as irritability, sweating, or seizures. Symptomatic infants
    will require IV calcium replacement.
    Infants who are large for gestational age should be examined closely for signs
    of birth trauma, such as cephalohematoma, clavicle fracture, and brachial plexus
    injury. Macrosomia in utero creates an increase in the intrauterine oxygen requirement, and the relative placental insufficiency leads to increased production of erythropoietin. The resultant polycythemia, defined as a central hematocrit greater than
    65 in a neonate, may give a ruddy or plethoric hue to the infant’s skin. Polycythemia
    contributes to elevated bilirubin levels and can cause hyperviscosity syndrome with
    resultant venous thrombosis in the renal veins, cerebral venous sinus, or mesenteric
    veins. Polycythemia is treated with increased hydration and in rare instances partial
    exchange transfusion