HYPOGLYCEMIA
Saturday, August 16, 2008
Essentials of Diagnosis & Typical Features
- Defined as blood glucose <>
- 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, irritability, 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
Therapy is based on provision of glucose either enterally or intravenously. Table 1–13 presents suggested treatment guidelines. In hyperinsulinemic states, boluses of glucose should be avoided and a higher glucose infusion rate used. After initial correction with a bolus of D10W, 2 mL/kg, glucose infusion should be increased gradually as needed from a starting rate of 6 mg/kg/min. Finally, in both IDMs and IUGR infants, those with high hematocrits and hypoglycemia are most likely to show clinical signs of hypoglycemia. In such infants, both the hypoglycemia and the polycythemia should be treated—with intravenous glucose infusion and partial exchange transfusion, respectively.
Prognosis
The prognosis of hypoglycemia is good if therapy is prompt. CNS sequelae are seen in infants with neonatal seizures resulting from hypoglycemia.
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, irritability, 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
Therapy is based on provision of glucose either enterally or intravenously. Table 1–13 presents suggested treatment guidelines. In hyperinsulinemic states, boluses of glucose should be avoided and a higher glucose infusion rate used. After initial correction with a bolus of D10W, 2 mL/kg, glucose infusion should be increased gradually as needed from a starting rate of 6 mg/kg/min. Finally, in both IDMs and IUGR infants, those with high hematocrits and hypoglycemia are most likely to show clinical signs of hypoglycemia. In such infants, both the hypoglycemia and the polycythemia should be treated—with intravenous glucose infusion and partial exchange transfusion, respectively.
Prognosis
The prognosis of hypoglycemia is good if therapy is prompt. CNS sequelae are seen in infants with neonatal seizures resulting from hypoglycemia.
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