Update-Neonatal Hypoglycemia

Written by David Wilson, MS, RNC The definition of neonatal hypoglycemia has varied over the past few decades and has generated considerable controversy. At the same time there has been the recognition that hypoglycemia may cause serious neurologic damage in infants.The subtle signs and symptoms of neonatal hypoglycemia and the variation of the presentation from one infant to another only serve to further complicate this issue. Common symptoms of neonatal hypoglycemia include lethargy, listlessness, poor feeding, thermoregulatory problems, apnea, cyanosis, jitteriness, tremors, seizure activity and respiratory distress. A working definition of neonatal hypoglycemia by Cornblath and Schwartz (1993) suggested a threshold of 40 mg/dl in the first 24 hours of life and 40-50 mg/dl thereafter for all infants. However, they specified that values below those did not imply neuroglycopenia or neurologic damage. Blood glucose levels are known to be in a dynamic state of fluctuation from birth. Several authors have presented normal serum glucose values for term infants who had not been fed formula or breast milk (Kalhan, 1993; Hawdon,1992) within the first few hours of life. These data were collected when it was traditional practice to keep healthy newborns NPO for several hours after birth. It is now common to allow breastfeeding shortly after delivery and formula is not withinfd for several hours. In 1994 Hawdon, Platt and Aynsley-Green suggested that serum glucose levels be maintained above 47 mg/dl (2.6 mmol/L) in infants at risk, i.e. those who are preterm, infants who are small for gestational age (SGA), infants of poorly controlled diabetic mothers, and any infant who suffers perinatal asphyxia. The researchers further pointed out the futility of screening seemingly healthy term infants for hypoglycemia since glucose levels have been shown to decrease shortly after birth and subsequently increase to maintain normoglycemia. Other studies of neonatal hypoglycemia have been published by Holtrop (1993) and Srinivisian and others (1986). Neonatal hypoglycemia may be caused by a number of factors. In infants of diabetic mothers (IDM) it is not uncommon for the infant to remain in a hyperinsulinemic state after losing the maternal glucose supply. Fetal glucose levels correspond to maternal levels as glucose crosses the placenta yet insulin production in the fetus begins early in gestation; insulin does not cross the placenta. When the IDM is deprived of maternal glucose the pancreas continues to produce insulin at the same fetal level and newborn glucose levels are rapidly depleted. This condition is usually transient and is treated either with early initiation of carbohydrate feedings or at times intravenous dextrose until the infant's metabolic adaptation is able to supply adequate amounts of glucose. In preterm infants and those born SGA adequate fetal glycogen storage has been interrupted or impaired, placing these infants at risk for hypoglycemia in the first several hours and days of life. Other perinatal events which may cause an increase in energy utilization (above those levels at which the newborn is able to supply glucose) include perinatal asphyxia, cold stress, respiratory distress, maternal corticosteroids, and prolonged labor. The newborn may also be at risk for hypoglycemia as a result of inborn errors of carbohydrate metabolism and amino acid metabolism (Brooks, 1997).

Pediatric Updates

Hyperinsulinism due to nesidioblastosis in the early neonatal period also is a cause for neonatal hypoglycemia (Starbuck,1997). A number of experts in the field of neonatology have recently explored the issue of neonatal hypoglycemia and have made recommendations for the revision of previous values for term and preterm infants to include higher parameters for defining hypoglycemia. These are partly due to studies that have demonstrated poor outcomes in neonates with previously acceptable glucose levels and updated technology which allows for the direct measurement of cerebral uptake and utilization of serum glucose. With increased magnetic resonance imaging of the neonatal brain the effects of hypoglycemia are also better understood .Koh and others (1988) demonstrated that children (including some infants) had abnormal brainstem auditory evoked potentials when serum glucose levels were below 47 mg/dl (2.6 mmol/L). The group of children with serum blood glucose levels above 47 mg/dl had normal neurologic function. This study also demonstrated that the severity of hypoglycemia did not necessarily correlate with symptoms as was previously believed. Data from Lucas, Morley, and Cole (1988) showed that preterm infants with glucose values below 47 mg/ dl over a period of several days had decreased neurodevelopmental scores (Bayley test) at 18 months follow up. This would seem to refute the idea that preterm infants can tolerate lower glucose values as has been postulated in the past. Aynsley-Green and Hawdon (1997) point out that there is no evidence to support the perception that the brain of the low birth weight infant is more resilient to low blood glucose levels than the term infant. Halamek and Stevenson (1998) recommend that a threshold of 45 mg/dl be utilized to screen and treat neonates for hypoglycemia. They further point out that while this may seem to be a parameter which may result in unnecessary treatment of some newborns it is prudent to err on the conservative side due to the lack of objective data and the consequences of nontreatment. McGowan, Hagedorn and Hay (1998) recommend that the previous levels defining hypoglycemia be abandoned in favor of levels of 47-50 mg/dl based upon the results of studies cited herein, changes in neonatal practice within past years and data which correlates lower levels of serum glucose with poor outcomes. Whether or not there will be consensus among other authorities to effectively increase the norms of serum glucose levels remains to be seen. The role of the nurse continues to be that of providing appropriate care for the newborn. In doing so the nurse must recognize the importance of reviewing the maternal and family history, and the delivery record for any factors which may place the infant at risk for hypoglycemia. Furthermore it is essential to evaluate the infant at risk for hypoglycemia regardless of presentation or lack of symptoms and to institute appropriate therapies for determining the necessity for subsequent monitoring of blood glucose levels or treatment. Nurse are in a unique position to ensure the newborn and family of continued wellness early in life.

References
Aynsley-Green A, Hawdon JM: Hypoglycemia in the neonate: current controversies. Acta Paediatr Jpn 39(Suppl 1):S 12-16,1997. Brooks C: Neonatal hypoglycemia. Neonatal Network 16(2):15-21,199 Cornblath M, Schwartz R: Hypoglycemia in the neonate. J Pediatric Endocrinology 6(2):113-129,1993. Halamek LP, Stevenson: Neonatal hypoglycemia, Part II: pathophysiology and therapy. Clinic Pediatr 37(1):11-16,1998. Hawdon JM, Platt MP, Aynsley-Green A: Patterns of metabolic adaptation for preterm and term infants in the first neonatal week. Arch Dis Child 67(4):357-365,1992.

Hawdon JM, Platt MP, Aynsley-Green A: Prevention and management of neonatal hypoglycemia. Arch Dis Child Fetal Neon Ed 70 (1):F60-F64,1994. Holtrop PC: The frequency of hypoglycemia in full-term large and small for gestational age newborns. Am J Perinatology 10(2):150-154,1993. Kalhan S: Metabolism of glucose and methods of investigation in the fetus and newborn. In Fetal and neonatal physiology, Polin RA and Fox WW, eds. Philadelphia: W.B. Saunders, 1993. Koh THH and others: Neural dysfunction during hypoglycaemia. Arch Dis Child 63:1353-1358,1988. Lucas A, Morley R, Cole TJ: Adverse neurodevelopmental outcome of moderate neonatal hypoglycaemia. Br Med J 297:1304-1308,1988. McGowan J, Hagedorn MIE, Hay WW: Glucose homeostasis, In Merenstein GB, Gardner S, eds. Handbook of Neonatal Intensive Care, ed. 4, St. Louis, Mosby, 1997. Srinivasan G and others: Plasma glucose values in normal neonates: a new look. J Pediatr 109 (1):114-117,1986. Starbuck AL: Nesidioblastosis: a case study. Neonatal Network 16(6):59-62,1997. See Chapter 9 in Essentials of Pediatric Nursing, 5th edition. See Chapters 9 & 10 in Nursing Care of Infants and Children, ed. 6.
March 15, 2002