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Neonatal hyperglycemia

Ann R Stark, MD
Rebecca Simmons, MD
Section Editors
Steven A Abrams, MD
Joseph I Wolfsdorf, MB, BCh
Deputy Editor
Melanie S Kim, MD


Glucose supply and metabolism are of central importance for growth and normal brain development in the fetus and newborn. Disorders in glucose availability or utilization can result in hypoglycemia or hyperglycemia.

The causes and management of neonatal hyperglycemia are reviewed here. Neonatal hypoglycemia is discussed separately. (See "Pathogenesis, screening, and diagnosis of neonatal hypoglycemia".)


Hyperglycemia — The definition of hyperglycemia is uncertain. It is often defined as blood glucose >125 mg/dL (6.9 mmol/L) or plasma glucose >150 mg/dL (8.3 mmol/L). However, these levels are frequently observed during glucose infusions in newborns, especially in extremely preterm infants, and may not require intervention [1].

Most neonatologists become concerned about hyperglycemia when plasma glucose concentration (the standard laboratory test) exceeds 180 to 200 mg/dL (10 to 11.1 mmol/L). However, higher levels of hyperglycemia are required to produce the hyperosmolality and osmotic diuresis that may be clinically important. Plasma osmolality increases by 1 mosmol/L for each 18 mg/dL increase in plasma glucose concentration. Thus, a rise in glucose concentration from 110 to 200 mg/dL (6.1 to 11.1 mmol/L) only increases osmolality by 5 mosmol/L, which is a relatively small change.

Glucosuria — Glucose excretion in the urine in hyperglycemic neonates is determined by the degree of hyperglycemia and renal tubular reabsorptive capacity for glucose. Newborns have variable reabsorptive capacities for glucose, which may be particularly reduced in those who are ill or preterm.


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Literature review current through: Jul 2017. | This topic last updated: Nov 29, 2016.
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