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26 - Hypoglycemia in the neonate
- from Section 4 - Specific conditions associated with fetal and neonatal brain injury
- Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California, Susan R. Hintz, Stanford University School of Medicine, California, Maurice L. Druzin, Stanford University School of Medicine, California
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- Book:
- Fetal and Neonatal Brain Injury
- Published online:
- 12 January 2010
- Print publication:
- 18 June 2009, pp 304-310
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Summary
Introduction
The mammalian fetus, in utero, is entirely dependent upon the mother for a continuous supply of glucose and other nutrients. Data from a number of studies in humans and animals have shown that under physiological circumstances there is no measurable production of glucose by the fetus, and that the entire glucose pool in the fetal compartment is derived from the mother. The transition from the intrauterine environment to an independent extrauterine life is associated with a number of metabolic and hormonal responses, which allow the vast majority of neonates to adapt to the extrauterine environment without any problem. Among the key events involved in this adaptation is the initiation of systemic glucose production, both from glycogenolysis and gluconeogenesis, in the period immediately after birth. Failure to adapt, as a consequence of alterations in maternal metabolism such as in diabetes in pregnancy, or as a consequence of metabolic problems in the neonate, may result in perturbations in glucose homeostasis leading to low blood glucose concentrations or hypoglycemia. It should be underscored that, during the initial period after birth, there is a decline in plasma glucose concentration from the cord blood levels in all infants, followed by an increase to a steady-state concentration. Although in the majority of infants this decrease in blood glucose concentration may be transient and inconsequential, in others it may be profound or persistent and lead to clinically serious problems involving significant neurological injury.
26 - Hypoglycemia in the neonate
- from Part IV - Specific Conditions Associated with Fetal and Neonatal Brain Injury
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- By Robert Schwartz, Division of Pediatric Endocrinology and Metabolism, Brown University School of Medicine Rhode Island Hospital, Providence, RI, USA, Marvin Cornblath, Division of Neonatology, Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, MD, USA, Satish C. Kalhan, Robert Schwartz Center for Metabolism and Nutrition, Metro Health Medical Center and Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA
- Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California
-
- Book:
- Fetal and Neonatal Brain Injury
- Published online:
- 10 November 2010
- Print publication:
- 06 February 2003, pp 553-570
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- Chapter
- Export citation
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Summary
Blood sugar measurements in neonates date back to the beginning of the twentieth century. By the 1920s it was known that concentrations of glucose were lower in premature (<2500 g birth weight) than in term infants, and both were less than those in older infants. In 1937, Hartmann and Jaudon first described a series of 286 neonates and infants with severe, recurrent, and/or persistent manifestations of hypoglycemia based on “true” blood sugar values. Their definitions distinguished between degrees of hypoglycemia based on the concept that all deviations from biological norms represent a continuum of abnormality. Thus, “mild” hypoglycemia was arbitrarily defined between 40 and 50 mg/dl (2.2–2.8 mmol/l); “moderate” between 20 and 40 mg/dl (1.1–2.2 mmol/l); and “extreme” less than 20 mg/dl (<1.1 mmol/l). These “true” blood sugar values were marginally greater than the blood glucose values measured today.
These classical reports stimulated little interest. Furthermore, no clinical significance was attributed to these variations in blood sugar values, even if extremely low (<20 mg/dl: 1.1 mmol/l). In fact, only isolated cases of hypoglycemic neonates, usually from postmortem examination, appeared until 1954, when McQuarrie reported his experience with familial recurrent severe hypoglycemia. In 1959, the report of transient symptomatic neonatal hypoglycemia in eight infants changed the concept and attitude to neonatal hypoglycemia. Significant clinical manifestations occurred with laboratory blood or spinal fluid glucose values <20–25 mg/dl, and cleared after restoring the blood glucose concentration to normal (>40 mg/dl).