neonatal hypoglycemia

HYPOGLYCEMIA


Defined as blood glucose <40–45 mg/dL.or below

LGA, SGA, preterm, and stressed infants at risk.

May be asymptomatic.

Infants can present with lethargy, poor feeding, irritability, or seizures.




General Considerations

Blood glucose concentration in the fetus is approximately 15 mg/dL less than the maternal glucose concentration. Glucose concentration normally decreases in the immediate postnatal period, with concentrations below 40–45 mg/dL being considered indicative of hypoglycemia. By 3 hours, the glucose concentration in normal-term babies stabilizes between 50 and 80 mg/dL. After the first few hours of life, concentrations below 40–45 mg/dL should be considered abnormal. The two most commonly encountered groups of term newborn infants at high risk for neonatal hypoglycemia are IDMs and IUGR infants.


Infants of Diabetic Mothers
The IDM has abundant glucose stores in the form of glycogen and fat but develops hypoglycemia because of hyperinsulinemia induced by maternal and fetal hyperglycemia. Other tissues also grow abnormally in utero, probably as a consequence of increased flow of nutrients from the maternal circulation. The result is a macrosomic infant who is at increased risk for trauma during delivery. Other problems related to the in utero metabolic environment include a cardiomyopathy (asymmetric septal hypertrophy), which can present as a murmur with or without cardiac failure and respiratory distress, and, more rarely, microcolon, which presents as low intestinal obstruction. Infants whose mothers have diabetes at conception are also at increased risk for congenital anomalies probably related to first-trimester glucose control. Other neonatal problems include a hypercoagulable state and polycythemia, a combination that predisposes the infant to large venous thromboses (eg, renal vein thrombosis). Finally, these infants are somewhat immature for their gestational age and are at increased risk for hyaline membrane disease, hypocalcemia, and hyperbilirubinemia.


Intrauterine Growth Restricted Infants
The IUGR infant has reduced glucose stores in the form of glycogen and body fat and therefore is prone to hypoglycemia despite relatively appropriate endocrine adjustments at birth. In addition to hypoglycemia, marked hyperglycemia and a transient diabetes mellitus-like syndrome may occasionally develop, particularly in the very preterm SGA infant. These problems can usually be handled by adjusting glucose intake, though insulin is sometimes needed transiently.


Other Causes of Hypoglycemia
Hypoglycemia occurs with disorders associated with islet cell hyperplasia (Beckwith-Wiedemann syndrome [macroglossia, omphalocele, macrosomia], erythroblastosis fetalis, nesidioblastosis), inborn errors of metabolism (glycogen storage disease, galactosemia), and endocrine disorders (panhypopituitarism, other deficiencies of counterregulatory hormones). It may also occur as a complication of birth asphyxia, hypoxia, or other stresses, including bacterial and viral sepsis. Premature infants are also at risk for hypoglycemia because of decreased glycogen stores.




Clinical Findings
The signs of hypoglycemia in the newborn infant are relatively nonspecific and may be subtle: lethargy, poor feeding, tability, tremulousness, jitteriness, apnea, and seizures. The disorder is most severe and resistant to treatment if due to hyperinsulinemia. Cardiac failure may occur in severe cases, particularly in IDMs with cardiomyopathy. Infants with hyperinsulinemic states can experience the onset of hypoglycemia very early (within the first 30–60 minutes of life).
Blood glucose can be measured by heel stick using a bedside glucometer. All infants at risk should be screened, including IDMs, IUGR infants, premature infants, and any infant with symptoms that could be due to hypoglycemia. All low or borderline values should be confirmed by direct measurement of blood glucose concentration determined in the laboratory.

It is important to continue surveillance of glucose concentration until the baby has been on full enteral feedings without intravenous supplementation for a 24-hour period. Relapse of hypoglycemia thereafter is unlikely.

Infants with hypoglycemia requiring intravenous glucose infusions for more than 5 days should be evaluated for the less common causes of hypoglycemia. This workup should include evaluation for inborn errors of metabolism, hyperinsulinemic states, and deficiencies of counterregulatory hormones.


Treatment.

When symptoms other than seizures are present, an intravenous bolus of 200?mg/kg (2?mL/kg) of 10% glucose is effective in elevating the blood glucose concentration. In the presence of convulsions, 4?mL/kg of 10% glucose as a bolus injection is indicated.
After initial therapy, a glucose infusion should be given at 8?mg/kg/min. If hypoglycemia recurs, the infusion rate and concentration should be increased until 15–20% glucose is used. If intravenous infusions of 20% glucose are inadequate to eliminate symptoms and maintain constant normal serum glucose concentrations, hyperinsulinemia is probably present and diazoxide should be administered. If the diazoxide is unsuccessful, octreotide may be useful; many infants with severe persistent hyperinsulinemic hypoglycemia undergo subtotal pancreatectomy. The serum glucose level should be measured every 2?hr after initiating therapy until several determinations are above 40?mg/dL. Subsequently, levels should be measured every 4–6?hr and the treatment gradually reduced and finally discontinued when the serum glucose value has been in the normal range and the baby asymptomatic for 24–48?hr. Treatment is usually necessary for a few days to a week, rarely for several weeks.
Infants at increased risk for hypoglycemia should have their serum glucose measured within 1?hr of birth, every 1–2?hr for the 1st 6–8?hr, and then every 4–6?hr until 24?hr of life. Normoglycemic high-risk infants should receive oral or gavage feeding with human milk or formula started at 1–3?hr of age and continued at 2–3?hr intervals for 24–48?hr. An intravenous infusion of glucose at 4?mg/kg/min should be provided if oral feedings are poorly tolerated or if asymptomatic transient neonatal hypoglycemia develops.