INTRODUCTION — 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 .
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.
The net effect is that glucosuria alone is not a good marker for hyperglycemia since it can occur at normal blood glucose concentrations. In one study of sick preterm infants born at 25 to 33 weeks gestation, for example, fractional glucose excretion varied widely and glucosuria was often seen at normal blood glucose concentrations . These variations presumably are related to immaturity of the proximal tubule.
On the other hand, mild hyperglycemia may be associated with little or no glucosuria in infants with mature proximal tubules. This was illustrated in a study of newborns who were given glucose infusions; at a mean blood glucose concentration of 197 mg/dL (11 mmol/L), there was little glucosuria and no significant osmotic diuresis .
PATHOGENESIS — Hyperglycemia typically occurs when a newborn cannot adapt to parenteral glucose infusion by decreasing endogenous glucose production or increasing peripheral glucose uptake . This is usually related to an associated clinical condition such as extreme prematurity or sepsis.
Normal glucose metabolism — In both term and preterm infants, the following observations of glucose metabolism are seen :
●Hepatic glucose production is suppressed by infusion of glucose (with or without amino acids), hyperglycemia, and insulin.
●Glucose production is not changed by intravenous (IV) lipid infusion.
●Circulating insulin concentrations increase appropriately with hyperglycemia and increase hepatic and peripheral glucose uptake.
Pathogenesis of hyperglycemia in preterm infants — Hyperglycemia is more common in preterm infants compared with term infants. Although the mechanism(s) for the increased risk of hyperglycemia in preterm infants is uncertain, the following may be contributory factors:
●Poor insulin response – Insulin responses may be inappropriately low in extremely low birth weight (ELBW) infants. In one study, 23 of 56 ELBW infants became hyperglycemic during IV glucose infusions that were incrementally increased to a maximum rate of 12 mg/kg per minute between days two and six of age . Baseline insulin levels were similar in hyperglycemic and euglycemic infants, but only 15 of 23 hyperglycemic infants had a normal insulin response.
The inappropriate insulin response in hyperglycemic ELBW infants may be related to defective islet beta cell processing of proinsulin. In a study comparing 15 hyperglycemic to 12 normoglycemic ELBW infants during the first week of life, proinsulin levels were significantly higher in the hyperglycemic ELBW infants, who also needed higher insulin levels to reach euglycemia compared with normoglycemic infants .
●Incomplete suppression of glucose production – Suppression of hepatic glucose production in response to glucose infusion also varies in very immature infants and may be incomplete. In a series of 10 infants born at 25 to 30 weeks gestation, glucose production rates decreased from 4.3 to 1.4 mg/kg per minute as glucose infusion was increased from 1.7 to 6.5 mg/kg per minute . Plasma concentrations of glucose and insulin also increased.
Proteolysis due to negative nitrogen balance, which occurs more commonly in the preterm infant, may also be a stimulus for inappropriate glucose production. For example, in ELBW infants, insufficient protein intake results in endogenous protein loss (proteolysis) in an effort to meet the basal metabolic needs of the infant.
●Increased secretion of counterregulatory hormones associated with stress – Secretion of epinephrine and cortisol in stressed infants may contribute to hyperglycemia. The role of stress was demonstrated in a report of metabolic responses to glucose infusion in preterm infants (weight 700 to 1550 g) . Measurements were made before and after infusion in controls and in infants who required assisted ventilation and were considered stressed. Stressed infants had higher levels of glucose and of cortisol compared with controls and were more likely to have hyperglycemia (13 of 18 versus 1 of 12 infants). This difference was not due to decreased insulin or increased cortisol levels, because, among the stressed infants, insulin levels were higher and cortisol levels lower in the hyperglycemic compared with the euglycemic newborns. (See "Physiologic response to hypoglycemia in healthy individuals and patients with diabetes mellitus", section on 'Counterregulatory hormones'.)
CAUSES — In general, neonatal hyperglycemia is associated with a clinical condition, rather than a specific disorder of glucose metabolism, and occurs in infants receiving intravenous (IV; parenteral) glucose infusions. A rare cause of hyperglycemia is neonatal diabetes mellitus.
Parenteral administration of glucose — Parenteral glucose is administered to most preterm or ill neonates because adequate enteral feeding is delayed. Neonatal hyperglycemia often occurs in this setting because of changes in glucose metabolism and requirements, leading to readjustment of glucose infusion rates. In neonates receiving parenteral administration of glucose, sepsis, prematurity, and stress are all factors that affect glucose metabolism and increase the risk of hyperglycemia.
Immediately after birth, parenteral glucose is typically provided at a rate of 5 to 8 mg/kg per minute to avoid hypoglycemia for neonates who will not be fed enterally. In most settings, sufficient glucose at a rate of 7 mg/kg per minute is provided by the administration of 10 percent dextrose solution at 100 mL/kg per day. Although dextrose is a hydrated form of glucose and is 91 percent glucose, the correction usually is not applied in clinical practice. The glucose infusion rate is increased to approximately 11 to 12 mg/kg per minute in the first two to three days after birth to provide calories for growth. In general, glucose infusion rates >15 mg/kg per minute are avoided, as this exceeds the ability of most infants to oxidize glucose and may promote excessive lipogenesis . (See "Parenteral nutrition in premature infants", section on 'Energy requirements'.)
Additional risk factors associated with hyperglycemia for infants who receive parenteral glucose includes increasing prematurity, intrauterine growth restriction, sepsis, and stress [1,9].
Prematurity — Hyperglycemia during glucose infusion is common in preterm infants and the risk increases with decreasing gestational age [9-12]. Extremely low birth weight (ELBW) infants (BW <1000 g) frequently develop hyperglycemia in the absence of high rates of glucose infusion . Proposed underlying mechanisms include reduced insulin secretion, incomplete suppression of hepatic glucose production, defective insulin secretion, and stress response resulting in counter hormone regulation . (See 'Pathogenesis' above.)
Sepsis — Hyperglycemia may be a nonspecific presenting sign of sepsis in an infant with previously normal blood glucose concentrations. Potential mechanisms include the stress response, decreased insulin release, and reduced peripheral utilization of glucose . In the very low birth weight preterm infant (birth weight <1500 g), fungal rather than bacterial sepsis appears to be more commonly associated with hyperglycemia .
Stress — The stress response to critical illness with the release of counter regulatory hormones (eg, epinephrine and cortisol) may result in hyperglycemia, especially in preterm infants who require mechanical ventilation. There is limited evidence that increased severity of respiratory distress and metabolic acidosis requiring medical intervention (eg, administration of bicarbonate) is linked to an increased risk of hyperglycemia . The stress response also may be responsible for hyperglycemia occurring after surgery. In this setting, increased rates of fluid administration containing dextrose may also be a contributory factor.
Drugs — Hyperglycemia is a common complication of glucocorticoid therapy, especially in ELBW infants . Hyperglycemia can also occur following administration of methylxanthines , phenytoin (the mechanism may be suppression of insulin release or insulin insensitivity)  and beta-adrenergic agents (eg, dopamine, epinephrine and norepinephrine) . Hyperglycemia is almost always mild in these cases and does not require therapy. If the infant is on IV fluids, the glucose infusion rate (GIR) can be reduced.
Neonatal diabetes mellitus — Neonatal diabetes mellitus (DM) is a rare cause of hyperglycemia. It is defined as persistent hyperglycemia occurring in the first months of life that lasts more than two weeks and requires insulin for management. Neonatal DM is a monogenic disorder caused by a mutation in genes that encode proteins that affect pancreatic beta cell function.
The etiology, evaluation and management of neonatal DM are discussed separately. (See "Neonatal diabetes mellitus".)
MANAGEMENT — Neonatal hyperglycemia is primarily observed in neonates receiving parenteral glucose infusion, especially preterm infants. As a result, management is focused on reducing glucose levels to target levels while maintaining adequate caloric intake for those patients who are dependent on parenteral nutrition.
Reduction of glucose infusion rate — Interventions to reduce the blood glucose concentration are initiated at values above 180 to 200 mg/dL (10 to 11.1 mmol/L). The first step in management is to decrease the parenteral glucose infusion rate. Reducing the rate to 4 to 6 mg/kg per minute usually lowers the blood glucose concentration. In most cases, this is accomplished by reducing the concentration of the dextrose solution from 10 to 5 percent. If provided with parenteral nutrition solution and lipid emulsion, infants can maintain normoglycemia with the reduced glucose supply by gluconeogenesis from the metabolism of glycerol and amino acids .
However, reducing the glucose infusion rate is a short-term solution because it results in decreased caloric intake and compromises growth. Glucose tolerance typically improves when enteral feedings are established. (See "Nutritional composition of human milk and preterm formula for the premature infant".)
Insulin therapy — Insulin improves glucose tolerance, allows provision of more calories, and promotes growth in infants who remain hyperglycemic at reduced glucose infusion rates. The exact indications for insulin therapy are not well defined. Most neonatologists, including the authors, would begin an insulin infusion in infants with persistent hyperglycemia (>200 to 250 mg/dL [11.1 to 13.9 mmol/L]) despite reductions in glucose infusion rate, and in infants who fail to thrive because of decreased glucose administration resulting in reduced caloric intake.
Small case series support the use of continuous insulin infusion to provide higher caloric input thereby promoting growth by safely increasing glucose infusion rates [5,21]. In infants receiving parenteral nutrition, improvement in glucose tolerance by continuous insulin infusion appears to be comparable with and without the addition of lipid emulsion .
Routine early insulin therapy — The routine early use of insulin therapy in preterm infants has been proposed to prevent catabolism, improve glucose control, and increase energy intake, which might improve growth. However, early insulin therapy does not appear to improve growth and, compared with standard care, may be associated with an increased risk of hypoglycemia and mortality at 28 days of age.
This was illustrated in a multicenter, open-label trial of 389 very low birth weight (VLBW) infants (BW <1500 g) who were randomly selected to receive either standard care for glycemic control or a parenteral infusion of 20 percent dextrose with early insulin therapy (0.05 units/kg per hour) starting within 24 hours of birth until seven days of age . The following findings were noted:
●The early insulin group had lower mean glucose levels compared with the standard care group (112 versus 121 mg/dL [6.2 versus 6.7 mmol/L]), were less likely to be hyperglycemic (defined as serum glucose greater than 180 mg/dL [10 mmol/L]) for more than 10 percent of the first week of life (21 versus 33 percent), were able to receive greater amounts of glucose infusion (51 versus 43 kcal/kg per day), and had less weight loss during the first week of life.
●More patients who received early insulin had episodes of hypoglycemia (29 versus 17 percent), which was defined as serum glucose levels less than 47 mg/dL (2.6 mmol/L) for more than one hour.
●There were no differences between the groups in the primary end point of mortality at the expected date of delivery or in the secondary end points of sepsis, necrotizing enterocolitis, retinopathy of prematurity, and growth parameters (ie, weight, length, and head circumference) at 28 days of age. However, the early insulin group had a higher mortality rate at 28 days of life.
This trial was ended early because of concerns of futility with regard to outcomes and concern for potential harm from insulin therapy. Follow-up assessment is ongoing to determine whether the increased incidence of hypoglycemia in the early insulin group had a detrimental effect on neurodevelopmental outcomes. (See "Management and outcome of neonatal hypoglycemia", section on 'Neurodevelopmental outcome'.)
Based upon these data, routine insulin therapy should not be used in VLBW infants prior to reducing glucose infusion rates. Insulin should be used to treat hyperglycemia when reducing the glucose infusion rate to approximately 6 mg/kg per minute is ineffective or not possible.
Risk of hypoglycemia — The blood glucose concentration should be monitored frequently during insulin infusion, although the risk of hypoglycemia appears to be small [24,25]. This was documented in a retrospective review of 34 extremely low birth weight (ELBW) infants (BW <1000 g) who developed hyperglycemia and glucosuria while receiving parenteral nutrition and were treated with insulin . Before therapy, mean blood glucose concentration was 195 mg/dL (11.1 mmol/L) while receiving glucose at a mean rate of 7.9 mg/kg per min. During insulin infusion, given for 1 to 58 days, blood glucose values of 25 to 40 mg/dL (1.4 to 2.2 mmol/L) were detected in fewer than 0.5 percent of samples (26 episodes of hypoglycemia in 7368 samples) and no values <25 mg/dL were seen. (See "Pathogenesis, screening, and diagnosis of neonatal hypoglycemia".)
Dose and target glucose levels — In neonates who receive insulin therapy, regular insulin (100 units/mL) is used and is usually diluted in normal saline to a concentration of 0.1 units/mL. In some centers, concentration of 0.5 units/mL is used. The solution should be changed every at least every 24 hours or based on the recommendations of the hospital pharmacy.
The initial step in management of a persistently elevated glucose level is administering a bolus insulin infusion via a syringe pump over 15 minutes at a dose between 0.05 and 0.1 units/kg. The blood glucose level is monitored every 30 to 60 minutes, and if it remains elevated, the insulin dose is repeated as a bolus every four to six hours. If the glucose level remains elevated after three bolus doses, a continuous infusion is suggested at an initial rate of between 0.01 and 0.05 units/kg per hour and is adjusted in small increments up to a maximum rate of 0.1 units/kg per hour to maintain glucose levels of 150 to 200 mg/dL (8.3 to 11 mmol/L). Tighter glycemic control aiming for glucose values substantially below 150 mg/dL (8.3 mmol/L) increases the risk of hypoglycemia .
Monitoring — The blood glucose concentration should be monitored within 30 minutes to 1 hour of the start of the infusion and after any change in the rate of glucose or insulin infusion. Glucose concentration should be monitored hourly until stable, and then less frequently.
Titration and discontinuation — As glucose tolerance improves, the insulin infusion should be tapered and discontinued to avoid hypoglycemia. In general, reductions in the insulin infusion rate can be made more rapidly than can increases. In our centers, infusion rates are decreased in increments of 0.01 to 0.05 units/kg per hour in response to glucose levels <150 mg/dL (8.33 mmol/L). Insulin infusion can be discontinued when the glucose level remains stable below 150 mg/dL (8.33 mmol/L) at the lowest infusion rate. The glucose level should continue to be monitored closely for the next 12 to 24 hours.
Adherence of insulin to plastic tubing — Plastic tubing used for infusion should be primed with insulin for at least 20 minutes before treatment because insulin nonspecifically binds to the tubing, resulting in decreased availability to the patient. In one report, recovery of insulin from effluent of primed polyvinyl chloride tubing at a flow rate of 0.2 mL/hour was greater at one, two, four, and eight hours compared with unprimed tubing (42, 85, 91, and 95 versus 22, 38, 67, and 75 percent, respectively) .
Amino acid and lipid infusion — Insulin infusion during euglycemia reduces proteolysis and protein synthesis in preterm infants who are not also given amino acids . This is in contrast to adults and children, in whom insulin increases protein synthesis. As a result, we suggest amino acid solution and lipid emulsion be administered to infants receiving glucose infusion to provide substrate for gluconeogenesis, spare glucose utilization, and stimulate insulin release, and enteral feedings are begun as soon as possible.
Although data are limited, a retrospective study demonstrated that nutritional changes resulting in greater protein and less fat and carbohydrates intake resulted in a lower mean blood glucose concentration and less frequent episodes of hyperglycemia, and no changes in the risk of hypoglycemia .
Enteral feeds — Enteral feeds promote the gastric release of glucose-dependent insulinotropic peptide (GIP) and GLP-1, incretin hormones that promote insulin secretion from the pancreas [30,31]. Gastrointestinal incretin-mediated insulin release in response to orogastric administration of a glucose load may occur when a threshold of glucose concentration has exceeded 105 mg/dL. (See "Approach to enteral nutrition in the premature infant".)
Our approach — In our center, for all infants receiving intravenous glucose infusions, amino acid solution and lipid emulsion are also provided as substrate for gluconeogenesis. Enteral feeding is initiated as soon as possible in order to wean and discontinue parenteral nutrition. (See 'Enteral feeds' above.)
Blood glucose monitoring is initiated for all patients receiving parenteral glucose. For infants with stable glucose concentration, daily monitoring is adequate. For ELBW, stressed, or septic infants who may not have a stable glucose concentration, or those receiving insulin infusion, more frequent monitoring is performed.
The following steps are taken to evaluate and manage hyperglycemia:
●Medications are reviewed and, if possible, drugs associated with high glucose levels are discontinued. These include glucocorticoids, phenytoin, and beta adrenergic agents.
●Patients are evaluated for possible sepsis. If clinically appropriate, blood cultures are obtained and empiric antibiotics are administered. (See "Clinical features, evaluation, and diagnosis of sepsis in term and late preterm neonates" and "Clinical features and diagnosis of bacterial sepsis in preterm infants <34 weeks gestation".)
●For patients who are receiving intravenous glucose infusions:
•In infants with blood glucose concentration greater than 180 to 200 mg/dL (10 to 11.1 mmol/L), the glucose infusion rate is decreased by reducing the concentration of infused dextrose4 to 6 mg/kg per minute, as long as the dextrose concentration does not go below 5 percent.
•Insulin therapy is initiated in neonates with persistent hyperglycemia (blood glucose >200 to 250 mg/dL [11.1 to 13.9 mmol/L]) despite reductions in glucose infusion rate, and in infants who fail to thrive because of decreased glucose infusion rates resulting in reduced caloric intake. Therapy is initially administered as a bolus of insulin administered via a syringe pump over 15 minutes as a dose between 0.05 and 0.1 units/kg. With the initiation of insulin, blood glucose level is monitored every 30 to 60 minutes until stable. (See 'Dose and target glucose levels' above.)
Continuous insulin infusion is used in infants with persistent hyperglycemia (blood glucose >200 to 250 mg/dL [11.1 to 13.9 mmol/L]) despite reductions in glucose infusion rate and after administering three insulin boluses. Infusion begins at a rate between 0.01 and 0.05 units/kg per hour, and is adjusted in small increments up to a maximum rate of 0.1 units/kg per hour to maintain blood glucose levels between 150 and 200 mg/dL. In the very preterm ill neonate, insulin may be given safely as long as the glucose concentration is monitored frequently because of the relatively wide heterogeneous response that occurs with IV administration. (See 'Insulin therapy' above.)
●Infusion insulin rates are decreased in increments of 0.01 to 0.05 units/kg per hour in response to glucose levels <150 mg/dL (8.33 mmol/L). Insulin infusion can be discontinued when the glucose level remains stable below 150 mg/dL (8.33 mmol/L) at the lowest infusion rate. The glucose level should continue to be monitored closely for the next 12 to 24 hours. (See 'Titration and discontinuation' above.)
OUTCOME — It is unclear if neonatal hyperglycemia is a clinically significant factor in neonatal outcome.
Observational data are conflicting as:
●Mortality and brain injury
•Several observational studies have reported that hyperglycemia in extremely preterm (EPT) infants (gestational age [GA] less than 27 weeks) was associated with an increased risk of mortality and brain injury including severe grade III and IV intraventricular hemorrhage [10,11,32-35]. In one study, insulin treatment was associated with a lower mortality rate at 28 and 70 days .
•In contrast, two studies did not find found an association between hyperglycemia and mortality or major morbidity [12,36].
•In a large observational study of 533 EPT infants, cognitive and motor assessment of 436 survivors at 6.5 years showed for each day with hyperglycemia (defined as >8 mmol/L [144 mg/dL]) there was a decrease of 0.33 points in Wechsler Intelligence Scale IQ (intelligence quotient) score and a decrease of 0.55 points in the Movement Assessment Battery score . Insulin therapy was not associated with either cognitive or motor outcome.
•In a retrospective analysis of data from 97 preterm infants (GA <32 weeks), persistent neonatal hyperglycemia (defined as blood glucose >150 mg/dL [8.33 mmol/L] for five or more days) was associated with decreased lean mass at four months postmenstrual age (PMA, n = 76 patients) and poorer scores on neurodevelopment testing at 12 months PMA (n = 66 patients) . However, this effect may have been mediated by low nutrient intake during the first week of life due to reduced glucose infusion rate to manage hyperglycemia.
Further information was provided by a clinical trial of 88 very low birth weight (VLBW) infants who were randomly selected to either standard or tight glycemic control . Assessment at seven years of age of 57 of the 77 survivors found similar survival rates without neurodevelopmental impairment between the tight and standard glycemic control groups . Children who were in the tightly controlled group had reduced height, increased height-adjusted lean mass, and reduced fasting blood glucose concentrations. However, the results of this trial are limited by the small number of patients.
Further research, including clinical trials to clarify the role of insulin, is needed to provide a better understanding of the consequences of hyperglycemia and determine which infants require intervention.
SUMMARY AND RECOMMENDATIONS
●Pathogenesis – Although the mechanisms are uncertain, the increased risk of hyperglycemia (defined as glucose levels >125 mg/dL [6.9 mmol/L]) in preterm infants compared with term infants is thought to be due to poorer insulin response, incomplete suppression of hepatic glucose production, and increased secretion of counterregulatory hormones associated with stress. (See 'Pathogenesis' above and 'Definition' above.)
●Causes – In general, neonatal hyperglycemia is caused by the administration of parenteral glucose, especially in very low birth weight (VLBW) infants (BW <1500 g). Other contributing conditions include the stress response to critical illness, sepsis, and drugs associated with hyperglycemia, such as phenytoin, glucocorticoids, and beta adrenergic agents. Rarely is neonatal hyperglycemia due to neonatal diabetes mellitus, which is caused by mutations in genes that encode for proteins that are involved with insulin synthesis or release from the pancreatic beta cells. (See 'Causes' above and "Neonatal diabetes mellitus".)
●Management – Blood glucose concentration should be monitored in all infants receiving intravenous glucose infusions. For most infants, daily monitoring is recommended until blood glucose concentration is stable. More frequent monitoring is recommended for extremely low birth weight (ELBW) infants (BW <1000 g), stressed or septic infants, or those receiving insulin infusion. (See 'Management' above.)
In our practice, a stepwise management approach for neonates whose blood glucose exceeds 180 to 200 mg/dL (10 to 11.1 mmol/L) includes the following (see 'Our approach' above):
•If possible, drugs that cause hyperglycemia are discontinued.
•For patients with signs and symptoms of sepsis, blood cultures are obtained and empiric antibiotics are administered. (See "Clinical features, evaluation, and diagnosis of sepsis in term and late preterm neonates" and "Clinical features and diagnosis of bacterial sepsis in preterm infants <34 weeks gestation".)
•For neonates receiving parenteral glucose infusion:
-The glucose infusion rate is reduced by decreasing the concentration of infused glucose, as long as the dextrose concentration does not go below 5 percent. (See 'Reduction of glucose infusion rate' above.)
-We suggest initial insulin therapy in neonates with persistent hyperglycemia (blood glucose >200 to 250 mg/dL [11.1 to 13.9 mmol/L]) despite reductions in glucose infusion rate and in infants who fail to thrive because of reduced caloric intake (Grade 2B). Therapy is initially administered as a bolus of insulin administered via a syringe pump over 15 minutes as a dose between 0.05 and 0.1 units/kg. (See 'Routine early insulin therapy' above.)
-We suggest continuous insulin infusion in infants with persistent hyperglycemia (blood glucose >200 to 250 mg/dL [11.1 to 13.9 mmol/L]) despite reductions in glucose infusion rate and administration of three insulin boluses (Grade 2C). Infusion begins at a rate between 0.01 and 0.05 unit/kg per hour and is adjusted in small increments up to a maximum rate of 0.1 units/kg per hour to maintain blood glucose levels between 150 and 200 mg/dL (8.3 to 11.1 mmol/L).
•Initiate enteral feeds as soon as possible.
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges See Wai Chan, MD, MPH, who contributed to an earlier version of this topic review.
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