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CHAPTER 15 Glucose Homeostasis
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449
IV therapy can be discussed with the parents before delivery so that they will be aware that the infant may require a longer hospital stay even if delivered at term.
If IV therapy is needed to treat neonatal hypoglycemia, regardless of cause, a thorough explanation of the treatment plan must be given to the parents at the time therapy is instituted.
Frequent progress reports should be provided to resolve unanswered (and often unasked) questions and relieve parental anxiety. When buccal dextrose
gel is utilized and infants are managed outside the NICU, parental teaching must include the need for additional observation and monitoring, the signs of hypoglycemia, and the need to avoid hypothermia. Parents of children with islet cell dysplasias need to be aware of the clinical signs of hypoglycemia and emergency treatment mea­sures that can be instituted, because recurrent
hypoglycemia may occur in these cases. Parents of infants with inborn errors of metabolism also need counseling with regard to prognosis and genetic counseling about risks for recurrence in future pregnancies.
HYPERGLYCEMIA
Definition of Neonatal Hyperglycemia
Hyperglycemia in newborns is usually defined, based on population data, as a blood glucose concentration of more than 125 mg/dL (greater than 150 mg/dL plasma) in a term infant or more than 150 mg/dL in blood in a preterm infant. In fetal life, the upper limit of the normal
range of glucose concentrations is 108 mg/dL. Unlike neonatal hypoglycemia, however, there are no reported “clinical” definitions of hyperglycemia (i.e., the appearance of physiologic disturbances asso­ciated with a specific high blood glucose concentra­tion). The incidence of statistically defined neonatal hyperglycemia is difficult to determine; estimates range from 5.5% of all infants receiving intravenous (IV) infusions of D10W to as high as 40% in infants weighing less than 1000 g who are receiving IV dextrose infusions. Dweck and Cassady48 noted that 86% of infants with birth weights under 1100 g were hyperglycemic, and of these infants, 84% had one or more serum glucose concentrations greater
100
than 300 mg/dL. In 2006, Blanco and colleagues19 found that 88% of infants with birth weights less than 1000 g had at least one blood glucose concen­tration greater than 150 mg/dL in the first week of life. Neonatal hyperglycemia has been increasing
in recent years in preterm infants as IV nutrition has become universal
140,159
but has been balanced more toward energy with relatively high IV infusion rates of dextrose and lipid.
163
Etiology of Hyperglycemia
Hyperglycemia is most common during the first week after birth (Box 15.3), although more
recent studies have shown that hyperglycemia in very-low-birth-weight (VLBW) infants can persist well after birth, even after weaning off TPN or IV dextrose infusion and well beyond the immediate postnatal “stress” period when hyperglycemia is most common.
Typically, a neonate with hyperglycemia is
an LBW infant (less than 32 weeks’ gestation and less than 1200 g birth weight)—often one with IUGR—who cannot tolerate an IV glu­cose infusion at the usual rate of 4 to 8 mg/ kg/min (i.e., D10W at 60 to 100 mL/kg/day).
This relative glucose intolerance appears to be caused by general immaturity of the usual regula­tory mechanisms. In immature infants, especially those with IUGR, these differences include fewer pancreatic islets and beta cells and decreased pan­creatic insulin secretion in response to glucose, a direct result of suppression by catecholamines both before and after birth.89 After birth, persistence of
BOX
15.3
• Iatrogenic (e.g., during intravenous glucose infusion)
• Decreased insulin production (e.g., with increased catecholamine production in very-low-birth-weight or intrauterine-growth-restricted infant; catecholamine infusion side effect)
• Decreased insulin sensitivity (e.g., with increased catecholamine pro­duction in very-low-birth-weight infant or transient diabetes mellitus; catecholamine infusion side effect)
• Sepsis
• Methylxanthine side effect
• Glucocorticoid side effect
140,146
ETIOLOGIC FACTORS IN NEONATAL HYPERGLYCEMIA
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catecholamine secretion can continue to suppress insulin secretion.31 Catecholamine excess also can lead to insulin resistance, both peripheral (leading to decreased glucose utilization) and hepatic (leading to increased glucose production), and peripheral glucose intolerance.48 Stress-induced production of cortisol and glucagon promote hepatic glycogen breakdown and gluconeogenesis with release of glucose into the circulation. These infants also have relatively decreased insulin-sensitive tissues (e.g., skeletal muscle and heart) as a fraction of body weight. There also is some evidence of abnormal insulin processing by the pancreatic beta cells such that more immature forms of insulin (proinsulin and proinsulin split products) are released. Because these immature forms of insulin are much less active in stimulating the insulin receptor, they may contrib­ute to a relative insulin resistance in these infants.
110
Some investigators also have reported that, unlike adults, most preterm and term infants fail to
suppress endogenous glucose production despite the administration of an adequate exogenous supply (e.g., IV infusion),
27,36,28
but other inves-
tigators did not measure any glucose production in premature infants receiving IV glucose at a rate of more than 2 mg/kg/min.
168
Hyperglycemia is most commonly iatrogenic in extremely low-birth-weight (ELBW) infants (less than 750 g) who require excess water to replace fluid lost through insensible water losses and who receive excess glucose along with the infused water because it is necessary to provide an iso­tonic IV solution. The risk for developing hyper­glycemia is significantly increased with decreasing birth weight (up to 18 times greater in infants with birth weights <1000 g than among those weighing 1000–2000 g) and with an increasing rate of glucose infusion, even if the absolute infusion
rate remains within the accepted range.
Delay in initiating enteral feedings may be an additional risk factor. The incidence of hyperglyce-
mia is higher in LBW infants receiving all of their nutrition parenterally than in those who receive at least a part of their nutrition enterally, and prolonged intravenous nutrition may contribute to insulin resistance, particularly when hypergly­cemia is present.
110,141
Enteral feeding increases
gut secretion of incretins (GLP-1 and GLP-2) that stimulate endogenous insulin secretion.
7
The rate at which the glucose concentration
is increased in IV solutions, including intravenous
nutrition, also may contribute. Hyperglycemia is
increasingly common at glucose infusion rates greater than 6 to 8 mg/kg/min (normal basal glucose utilization rates are 4 to 6 mg/kg/min).
The presence of illness (e.g., sepsis), treatment with corticosteroids, and RDS that requires mechanical ventilation are associated with increased risk for developing hyperglycemia, most likely because of increased circulating catecholamine and cortisol concentrations that lead to increased lipolysis and glycogenolysis and inhibit pancreatic insulin secre­tion and insulin action.
Several other etiologic factors must be considered
in infants with hyperglycemia. Increased blood
glucose concentrations have been reported in association with sepsis.16 Intravenous lipid infu­sions also contribute to hyperglycemia by simple mass action of competitive lipid carbon supply to the mitochondria
144
and by glycerol that is
a component of IV lipid emulsions. effects are worsened if given rapidly at rates of more than 0.25 g/kg/hr, but current practice is
to administer lipids at a slower rate.
164
Lipid oxi­dation in hepatocytes also produces cofactors (e.g., ATP, NADP, NADPH, acetyl Co-A) that activate and fuel gluconeogenesis.
58,113
Methylxanthines
are frequently used to treat apnea in preterm infants and may be a cause of hyperglycemia.
This problem has been well documented after the­ophylline overdose but may occur also with appro­priate administration. One study, for example, found that blood glucose concentrations in infants with therapeutic theophylline levels were higher than in untreated control subjects, with glucose concen­trations in the hyperglycemic range in two treated
138
infants.
Neonates undergoing surgical procedures also are at increased risk for hyperglycemia, proba­bly because of a combination of the large quantities of glucose-containing fluids and blood products that may be administered during the procedure and the effects of stress-related hormones. Infusions of catecholamines and glucocorticoids compound the effects of stress production of these hormones on inhibiting insulin secretion, promoting hepatic glucose production, and reducing peripheral insulin action and glucose intolerance.
Neonatal Diabetes
Neonatal diabetes is rare, and 40% to 50% of cases are due to transient neonatal diabetes mellitus
143
Such
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(TNDM). TNDM is associated with IUGR and may be difficult to distinguish from hyperglyce­mia due to increased levels of catecholamines and other stress hormones and related decreased insu­lin secretion and sensitivity. Genetic mutations or epigenetic anomalies in the chromosome region 6q24 have been identified in 70% of patients with TNDM.
132,151
In TNDM, unlike true diabetes mellitus, ketosis does not develop. Most cases self-resolve, but insulin therapy may be necessary. Permanent neonatal diabetes mellitus (PNDM) also occurs, although this is a rare disorder, with inci­dence estimated at 2 to 3 per 100,000 live births. Only about 25% of infants with PNDM have IUGR. Causes include mitochondrial diseases, pan­creatic hypoplasia or aplasia, abnormal pancreatic glucokinase activity, and mutations of pancreatic K
channel. Neonatal diabetes may be associated
ATP
with other abnormalities including developmental delay, skeletal dysplasias, and intestinal atresia.
Prevention of Hyperglycemia
Recognition of those infants at risk for dis­turbances in glucose homeostasis is the most important step in preventing hyperglycemia.
Hyperglycemia occurs most often in preterm infants receiving high rates of IV glucose. In a
VLBW infant, hyperglycemia may be avoided by starting IV glucose infusions at rates of 2 to 3 mg/kg/min and checking blood glucose concentrations frequently (as often as every 3 to 4 hours) while the infant continues to receive IV glucose.
140
There is some evidence that
starting amino acid infusions shortly after birth in very preterm infants may limit the develop­ment of hyperglycemia, perhaps by increasing
insulin production and secretion and also by pro­moting protein turnover and its attendant glucose (energy) requirements.
17,22,156
As noted, introduc-
tion of small-volume enteral feedings as soon
as possible may also reduce the incidence or duration of hyperglycemia in VLBW infants by
stimulating incretin secretion and increasing glucose metabolism.
7,81
Clinical Signs
Hyperglycemia usually is asymptomatic and most often is diagnosed on routine screening of the infant at risk. It should be suspected in
any preterm infant, and is likely to be more exag­gerated the more preterm the infant. It also should be suspected in infants who had hypoxic-ischemic conditions shortly before or during birth and in any sick or physiologically unstable infant.
If a problem with glucose homeostasis is sus­pected, documentation of the aforementioned data, history, physical examination, and clinical signs must reflect ongoing monitoring and mea­sures taken.
LABORATORY DATA
Plasma (serum) glucose concentrations should be measured in any infant as soon as possible after starting IV dextrose (alone or as part of TPN). These measurements should be continued at reasonable frequencies depending on whether hyperglycemia is found and is very high or highly variable. During treatment, measurement contin­ues until normal values are achieved and main­tained for reasonable periods. Since hyperglycemia can persist in very preterm infants even after IV dextrose infusions have been discontinued, inter­mittent glucose concentrations should be mea­sured for several days after stopping IV dextrose infusions or TPN. Persistent hyperglycemia has been associated with worse morbidities and even mortality and should not be allowed to continue. Enteral feeding is the best treatment, as it pro­motes secretion of incretins from the gut, which stimulate insulin secretion.
Treatment of Hyperglycemia
GLUCOSE
Most cases of hyperglycemia can be treated by reducing the neonate’s IV glucose infusion rate. This approach, when combined with other
measures such as early use of IV amino acids and early enteral feeding with reasonably rapid feeding advancement, commonly reduces glucose con­centrations into more acceptable ranges within 24 hours. Many LBW infants will tolerate glucose
infusions at rates as low 4 mg/kg/min with normal glucose concentrations, although Zarif and colleagues of infants weighing less than 1000 g had a blood glucose concentration higher than 125 mg/dL while receiving glucose at an average rate of 4.4 mg/kg/min. VLBW infants with high
fluid requirements resulting from large insensible
167
reported that more than 40%
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water losses through the skin may require a com­bination of water and glucose intake that could be administered only by using a hypotonic solution such as D
W to avoid hyperglycemia. The use of
2.5
a low glucose concentration in the IV infusate necessitates the addition of sodium (e.g., D
2.5
W has approximately 130 mOsm/L, requiring the addition of sodium chloride to produce an isotonic solution with 280 mOsm/L), which may further complicate management of fluids and electrolytes. Another approach is to continue a lower fluid rate of IV dextrose infusion with D5W but infuse sterile water through a gastric tube to meet fluid needs. A VLBW infant needs adequate caloric intake
(50–60 kcal/kg/day) to avoid a negative nitro­gen balance and tissue catabolism. These needs often cannot be met without resultant hypergly­cemia. If the glucose is only mildly elevated (e.g.,
concentrations of 125–150 mg/dL) and the infant has no evidence of contributing adverse pathologic conditions, reducing the rate of IV glucose admin­istration may not be necessary, as long as amino acid infusions and enteral feeding are increased, as they generally promote insulin secretion and incretin production and promote glucose utilization. There is little evidence, however, to determine whether this practice will lead to better or worse longer term neurodevelopmental outcomes. Regardless, such infants should have repeated glucose measurements made to ensure that the hyperglycemia resolves.
LIPID AND AMINO ACIDS
Intravenous lipid infusion rates can be decreased to help reduce hyperglycemia. This limits the
contribution of FFAs produced by lipid metabolism that, on oxidation, generate energy to drive gluco­neogenesis (acetyl CoA and reducing equivalents, NAD/NADH). Decreasing lipid supply also limits the competition of fatty acids with glucose for oxi­dation and the direct enhancement of gluconeogenic enzymes in the liver and thus the production of glu­cose. Limiting lipid supply also reduces the supply of glycerol, which is the primary support for glucone­ogenesis in newborn infants. As with reducing the
glucose infusion rate, reducing lipid infusion rates also reduces energy supply. The risks of reducing
energy intake to lower glucose concentrations, versus those of the hyperglycemia itself, are uncertain.
Amino acid infusions should be started early to promote insulin secretion and enhance pro­tein turnover with its obligatory energy (hence,
glucose) requirements.
22,156
Amino acids do not contribute measurably to enhancing gluconeogen­esis, even though they provide more substrate.
INSULIN INFUSION
144
Because of the foregoing considerations, some authors have suggested the use of a continuous
insulin infusion in the infant who cannot toler­ate infusion of glucose solutions with concen­trations greater than 5 g/dL (e.g., D5W).
18,46
Infusion of insulin at rates of 0.2 to 0.8 mU/kg/ min (0.01 to 0.05 U/kg/hr) for 12 to 24 hours may improve glucose tolerance. However, insulin
avidly binds to plastic IV tubing; thus the actual rate of insulin administration may be difficult to deter­mine and may vary over time. Although various methods have been proposed, such as priming the tubing with insulin-containing solution or albu­min, these have not been shown to be consistently effective.
149
Hypoglycemia during administration of exog­enous insulin can be avoided by starting with a low infusion rate (0.05 to 0.1 mU/kg/min) and increasing the rate by 10% to 20% every 60 to 90 minutes until the glucose concen­tration is less than 200 mg/dL. Blood glucose concentrations should be monitored every 15 to 20 minutes during initiation of the insulin infusion, and an IV glucose infusion should be maintained to avoid any abrupt changes in blood glucose concentration and to allow rapid correction of glucose concentration if it starts to fall below “normal” values. Use of insulin infusion has been reported to improve tolerance to glucose infusions, resulting in increased car­bohydrate intake and weight gain.
4,15
Most of
the weight gain is fat, however, and there is risk
for fatty infiltration and secondary inflammation in the liver and heart when insulin and glucose infu­sions are maintained for long periods. Such insulin treatment inhibits glucose production, though not as readily as in adults.27 The effect of insulin to pro­mote glucose utilization is modest in very preterm infants, given the small amount of insulin-sensitive tissue (primarily skeletal muscle) per body weight. Acutely, insulin infusion has been noted to
increase lactate production, with lactate concen­trations up to threefold greater than baseline, and may be associated with metabolic acidosis.
Administration of glucose and insulin at high rates also enhances CO2 production, which might lead
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to hypercarbia in infants with respiratory disease. Also, episodes of hypoglycemia can occur even with careful monitoring during insulin infusion. The use
of insulin to prevent hyperglycemia in neonates has been evaluated in a randomized prospec­tive prophylactic study that showed no obvious benefit and considerable morbidity, particularly a significant increase in the incidence of hypo­glycemic episodes. The authors of this study and
an editorial commentary concluded that chronic
insulin infusion cannot be recommended and must be used cautiously even in cases of acute hyperglycemia.
15,78
This is especially true because there are no clinical studies that have demonstrated a cause-and-effect relationship between brief peri­ods of neonatal hyperglycemia and adverse long­term outcomes, and long-term neurodevelopmental outcomes are not necessarily adversely affected by neonatal hyperglycemia in preterm infants.
158
Theoretically, hyperglycemia can induce an osmotic diuresis, and close attention should be paid to fluid balance in the hyperglycemic infant. However, this is rarely seen at blood glucose
concentrations less than 400 mg/dL or when hyper­glycemia occurs intermittently and for brief periods. Finally, as in hypoglycemia, efforts should be made to treat any underlying etiology, such as sepsis.
Two recent studies, one in neonatal lambs and
one in extremely preterm infants with chronic
hyperglycemia, have shown reduced mortality when insulin was used to reduce plasma glucose concentrations.
5,166
These studies did not include subjects who had their glucose concentrations lowered by other means. Thus, it remains unclear whether insulin itself has a specific beneficial effect on lowering mortality or whether it is just one approach to lowering glucose concentrations and avoiding their adverse effects. A Cochrane Review
of one study showed that insulin infusion versus reduced glucose infusion to treat hypergly­cemia in ELBW preterm infants showed no difference between groups in all age/weight groups on death, sepsis, retinopathy of pre­maturity, necrotizing enterocolitis, intracranial hemorrhage, chronic lung disease, NICU days, or growth.
104,134
Insulin should be used with
caution, therefore, and only when safer and more conventional approaches to lowering glucose concentrations have failed.69 Insulin
actually makes the infant fatter and contributes to excess mitochondrial carbon load and production of
reactive oxygen species. Insulin does not increase
glucose uptake by the brain or enhance neuro­nal growth or dendritic development—in fact, it
might do just the opposite (see later). It does not
increase linear growth or consistently increase lean mass growth when given in excess of nor­mal physiologic doses; positive effects are only
found to a minimal extent when the insulin is accompanied by protein.
Complications of Hyperglycemia
Although there is no direct evidence, hypergly-
cemia in the preterm infant has been postu­lated to increase the risk for IVH by causing rapid changes in osmolarity with resultant rapid
fluid shifts within the brain and germinal matrix. Increased mortality rate in hyperglycemic prema­ture infants compared with their normoglycemic counterparts has been reported, although hyper­glycemia may have been a marker for those infants with more severe illness rather than a direct cause of the increased mortality rate.2 Osmotic brain
injury and death have occurred in infants acci­dentally infused IV with an erroneously high dextrose solutions, such as D75W rather than D
W. Increased morbidity may be seen in the
7.5
form of greater difficulty with fluid and electrolyte management because use of dextrose-containing fluids must be limited and problems establishing adequate nutrition. Several studies also suggest an
association between hyperglycemia in ELBW infants and increased incidence of retinopathy of prematurity,
production of reactive oxygen species and reduced angiogenesis and secondary neuronal necrosis, but no definitive cause-and-effect relationship has been demonstrated as of yet.
Complications of hyperglycemia are increas­ingly recognized in adults and children in ICUs, and many of the associated morbidities are seen in newborn infants even if not considered to be caused by hyperglycemia. Such morbidi­ties include increased morbidity and mortality, impaired immunity and increased rates of infec­tion, poor wound healing, suppressed autophagy, diminished cellular repair and organ recovery, and loss of skeletal and cardiac muscle. Enteral
feeding rather than continued IV feeding has been most successful in preventing or reversing these problems. Similar evidence in
29,55,111
perhaps due to increased
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preterm infants is less clear. Other established effects of marked hyperglycemia are documented in preterm infants, including increased energy expenditure, increased O2 consumption, increased CO2 production with tachypnea, increased fat deposition in excess of lean mass, increased fatty infiltration with inflammation in the heart and liver, increased risk of deep venous thrombosis due to suppressed anticoagulant proteins and increased procoagulant proteins, risk of right ventricular dysfunction, interventricular septal hypertrophy, amplified sympathetic nervous and renin-angiotensin-aldosterone systems, increased health care–associated infections,
169
and accumu­lation of myocardial collagen and fibrosis from excessive production of free radicals.
24,114,118,147
There also is the potential for increased bac-
terial sepsis with persistent hyperglycemia, as
bacteria thrive with excess glucose, leading to worse infections and death of the organism. In
the NICU, where bacterial infections are more common as causes of serious sepsis, normal to low-normal plasma glucose may be protec-
165
tive.
Hyperglycemia also worsens outcomes
in infants with hypoxic ischemic encepha­lopathy, even more so than hypoglycemia.13
Perhaps more worrisome are animal studies that demonstrate marked adverse effects of chronic and marked hyperglycemia in fetuses and neonates
on neural development (reduced numbers of dendritic spines and synapse formation),74 and
decreased neuronal density, increased oxidant sta­tus, and decreased antioxidant status in the brain along with increased mortality.
150
Clinical stud-
ies in preterm infants also have shown that growth may or may not be affected (increased or decreased) with prolonged hyperglycemia in VLBW preterm infants, but linear growth is reduced,4 perhaps due to down regulation of
the growth hormone axis, and such poor growth
is associated with reduced cognitive develop-
126
ment.
Most worrisome are continued reports of associations between severe hyperglycemia (two or more consecutive blood glucose concentrations greater than 216 mg/dL at least 3 hours apart) as part of early enhanced TPN in ELBW preterm
infants and increased mortality, as early as the first day of life and even after 7 days.
140,161
Infants with TNDM usually recover sponta­neously within the first week; persistent insulin resis­tance is extremely rare. However, those infants with
chromosomal mutations have an increased incidence of adult-onset diabetes later in life.
132
No neurologic sequelae have been directly attributed to the presence of transient hyperglycemia in these neonates.
ACKNOWLEDGMENTS
Supported by NIH grants R01 DK088139 (PJR, PI; WWH, Co-I); Bill and Melinda Gates Foundation Grand Challenges Exploration Grant OPP1061082 (WWH, PI); NIH Training Grant T32 HD007186-32 (WWH, PI and PD); NIH K12 HD068372 (WWH, PD); NIH UL1TR001082 (WWH, Co-PD).
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