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Cornblath M, Hawdon J, Williams A et al. Pediatrics 2000;105:1141-1145

A direct quote from this paper summarizes the state of knowledge about the clinical entity: "However, it is not possible to define a blood glucose level that requires intervention in every newborn because there is uncertainty over the level and duration of hypoglycemia that cause damage, and little is known of the vulnerability, or lack of it, of the brain of infants at different gestational ages for such damages."

The distinguished authors of this paper do discuss much of interest about glucose metabolism in the newborn. Typical manifestations of neonatal hypoglycemia are very non-specific and include the following: irritability, lethargy, apnea, cyanosis, poor feeding, hypotonia, tremor and seizures. The following triad is mentioned in the paper as essential in the diagnosis of hypoglycemia: 1. the presence of characteristic manifestations, 2. coincident with an accurate, measurement, and 3. the resolution of the manifestations with the establishment of normoglycemia. There is little information on acute endocrine and metabolic responses to low glucose in the newborn and even less long-term follow-up of asymptomatic infants who had low glucose measurements.

In reviewing the adaptation to extrauterine life vis-a-vis glucose, the newborns plasma glucose starts at 60%-80% of the maternal level, declines for 2 hours then increases to a steady state in the first 3 hours after birth as newborn liver releases 4-6 mg/kg/min glucose. Even though glucose is the major source of energy for the brain, other sources such as ketone bodies, lactate and possibly amino acids are oxidized by neonatal brains. It seem clear that the neonate has the ability to mobilize fatty acids and form ketone bodies and there is evidence for increased rates of lipolysis and fatty acid oxidation in the preterm newborn. The availability of alternate sources of energy further clouds the significance of a single measurement of glucose in the newborn.

The authors recommend intervention in newborns who show clinical signs as mentioned above and whose plasma glucose measures < 45 mg/dl. The interventions recommended include IV administration of glucose for plasma levels < 25 mg/dl. There is some data that preterm infants whose plasma glucose was measured at < 47 showed some neurological abnormalities at 1/5 and 7 years but the information was obtained from a retrospective review. Glucose measurement using reagent strips was considered to be useful only as a screen. The authors strongly recommend that the diagnosis of hypoglycemia be confirmed with at least one reliable plasma measurement.

Comment: I enjoyed this relatively short paper on glucose and energy metabolism in the newborn as well as the discussion of the difficulty in determining at exactly what plasma level of glucose a newborn is at risk for neurologic damage. However, it was certainly not written with a pediatric anesthesiologist in mind. Virtually none of the clinical signs of hypoglycemia mentioned in the paper can be detected in the anesthetized newborn. We will always be left treating a number and only a number while we care for children in the operating room. Based on this paper, I feel comfortable using a plasma glucose measurement of 45-50 mg/ as an operational threshold for intervention.

Reviewed by: Thomas J. Mancuso, MD, FAAP
Children's Hospital, Boston, MA