Clinical Report—Postnatal Glucose Homeostasis inLate-Preterm and Term Infants

abstractThis report provides a practical guide and algorithm for the screeningand subsequent management of neonatal hypoglycemia. Current evi-dence does not support a specific concentration of glucose that candiscriminate normal from abnormal or can potentially result in acuteor chronic irreversible neurologic damage. Early identification of theat-risk infant and institution of prophylactic measures to prevent neo-natal hypoglycemia are recommended as a pragmatic approach de-spite the absence of a consistent definition of hypoglycemia in theliterature. Pediatrics 2011;127:575–579

INTRODUCTIONThis clinical report provides a practical guide for the screening andsubsequentmanagement of neonatal hypoglycemia (NH) in at-risk late-preterm (34–366⁄7 weeks’ gestational age) and term infants. An expertpanel convened by the National Institutes of Health in 2008 concludedthat there has been no substantial evidence-based progress in definingwhat constitutes clinically important NH, particularly regarding how itrelates to brain injury, and that monitoring for, preventing, and treat-ing NH remain largely empirical.1 In addition, the simultaneous occur-rence of othermedical conditions that are associatedwith brain injury,such as hypoxia-ischemia or infection, could alone, or in concert withNH, adversely affect the brain.2–5 For these reasons, this report doesnot identify any specific value or range of plasma glucose concentra-tions that potentially could result in brain injury. Instead, it is a prag-matic approach to a controversial issue for which evidence is lackingbut guidance is needed.

BACKGROUND

Blood glucose concentrations as low as 30 mg/dL are common inhealthy neonates by 1 to 2 hours after birth; these low concentrations,seen in all mammalian newborns, usually are transient, asymptomatic,and considered to be part of normal adaptation to postnatal life.6–8

Most neonates compensate for “physiologic” hypoglycemia by produc-ing alternative fuels including ketone bodies, which are released fromfat.

Clinically significant NH reflects an imbalance between supply and useof glucose and alternative fuels and may result from a multitude ofdisturbed regulatory mechanisms. A rational definition of NH mustaccount for the fact that acute symptoms and long-term neurologicsequelae occur within a continuum of low plasma glucose values ofvaried duration and severity.

David H. Adamkin, MD and COMMITTEE ON FETUS ANDNEWBORN

KEY WORDSnewborn, glucose, neonatal hypoglycemia, late-preterm infant

ABBREVIATIONSNH—neonatal hypoglycemiaD10W—dextrose 10% in water

This document is copyrighted and is property of the AmericanAcademy of Pediatrics and its Board of Directors. All authorshave filed conflict of interest statements with the AmericanAcademy of Pediatrics. Any conflicts have been resolved througha process approved by the Board of Directors. The AmericanAcademy of Pediatrics has neither solicited nor accepted anycommercial involvement in the development of the content ofthis publication.

The guidance in this report does not indicate an exclusivecourse of treatment or serve as a standard of medical care.Variations, taking into account individual circumstances, may beappropriate.

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The authors of several literature re-views have concluded that there is nota specific plasma glucose concentra-tion or duration of hypoglycemia thatcan predict permanent neurologic in-jury in high-risk infants.3,9,10 Data thathave linked plasma glucose concentra-tionwith adverse long-termneurologicoutcomes are confounded by variabledefinitions of hypoglycemia and its du-ration (seldom reported), the omis-sion of control groups, the possible in-clusion of infants with confoundingconditions, and the small number ofasymptomatic infants who were fol-lowed.3,11,12 In addition, there is no sin-gle concentration or range of plasmaglucose concentrations that is associ-ated with clinical signs. Therefore,there is no consensus regarding whenscreening should be performed andwhich concentration of glucose re-quires therapeutic intervention in theasymptomatic infant. The generallyadopted plasma glucose concentra-tion that defines NH for all infants(�47 mg/dL) is without rigorous sci-entific justification.1,3,4,9,12

WHICH INFANTS TO SCREEN

Because plasma glucose homeostasisrequires glucogenesis and ketogene-sis to maintain normal rates of fueluse,13 NH most commonly occurs in in-fants with impaired glucogenesisand/or ketogenesis,14,15 which may oc-cur with excessive insulin production,altered counterregulatory hormoneproduction, an inadequate substratesupply,14–16 or a disorder of fatty acidoxidation.15 NH occurs most commonlyin infants who are small for gesta-tional age, infants born to motherswho have diabetes, and late-preterminfants. It remains controversialwhether otherwise normal infantswho are large for gestational age areat risk of NH, largely because it is diffi-cult to exclude maternal diabetes ormaternal hyperglycemia (prediabe-

tes) with standard glucose-tolerancetests.

A large number of additional maternaland fetal conditions may also place in-fants at risk of NH. Clinical signs arecommon with these conditions, and itis likely that patients with such a con-dition are already being monitoredand that plasma glucose analyses arebeing performed.13,17 Therefore, forpracticality, “at risk” in the manage-ment approach outlined in Fig 1 in-cludes only infants who are small forgestational age, infants who are largefor gestational age, infants who wereborn to mothers who have diabetes,and late-preterm infants. Routinescreening andmonitoring of blood glu-cose concentration is not needed inhealthy term newborn infants after anentirely normal pregnancy and deliv-ery. Blood glucose concentrationshould only be measured in term in-fants who have clinical manifestationsor who are known to be at risk. Plasmaor blood glucose concentration shouldbemeasured as soon as possible (min-

utes, not hours) in any infant whoman-ifests clinical signs (see “ClinicalSigns”) compatible with a low bloodglucose concentration (ie, the symp-tomatic infant).

Breastfed term infants have lower con-centrations of plasma glucose buthigher concentrations of ketone bodiesthan do formula-fed infants.13,17 It is pos-tulated that breastfed infants toleratelower plasma glucose concentrationswithoutanyclinicalmanifestationsorse-quelae of NH because of the increasedketone concentrations.8,12–14

WHEN TO SCREEN

Neonatal glucose concentrations de-crease after birth, to as low as 30mg/dL during the first 1 to 2 hours af-ter birth, and then increase to higherand relatively more stable concentra-tions, generally above 45 mg/dL by 12hours after birth.6,7 Data on the optimaltiming and intervals for glucosescreening are limited. It is controver-sial whether to screen the asymptom-atic at-risk infant for NH during this

FIGURE 1Screening for and management of postnatal glucose homeostasis in late-preterm (LPT 34–366⁄7weeks) and term small-for-gestational age (SGA) infants and infants who were born to mothers withdiabetes (IDM)/large-for-gestational age (LGA) infants. LPT and SGA (screen 0–24 hours), IDM and LGA�34 weeks (screen 0–12 hours). IV indicates intravenous.

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normal physiologic nadir. No studieshave demonstrated harm from a fewhours of asymptomatic hypoglycemiaduring this normal postnatal periodof establishing “physiologic glucosehomeostasis.”9

Infants born to mothers with diabetesmay develop asymptomatic NH as earlyas 1 hour after birth18 and usually by 12hours of age.18 In contrast, infants whoare large for gestational age or smallfor gestational age may develop lowplasma glucose concentrations at asearly as 3 hours of age,19 and theseinfantsmay be at risk of NH for up to 10days after birth.20 Therefore, at-risk in-fants should be screened for NH with afrequency and duration related to riskfactors specific to the individual in-fant.5 Screening the asymptomatic at-risk infant can be performed withinthe first hours of birth and continuedthroughmultiple feed-fast cycles. Late-preterm infants and infants who aresmall for gestational age should be fedevery 2 to 3 hours and screened beforeeach feeding for at least the first 24hours. After 24 hours, repeatedscreening before feedings should becontinued if plasma glucose concen-trations remain lower than 45 mg/dL.

LABORATORY DATA

When NH is suspected, the plasma orblood glucose concentration must bedetermined immediately by using oneof the laboratory enzymatic methods(eg, glucose oxidase, hexokinase, ordehydrogenase method). Plasmablood glucose values tend to be ap-proximately 10% to 18% higher thanwhole-blood values because of thehigher water content of plasma.21,22

Although a laboratory determination isthe most accurate method of measur-ing the glucose concentration, the re-sults may not be available quicklyenough for rapid diagnosis of NH,which thereby delays the initiation oftreatment.23 Bedside reagent test-strip

glucose analyzers can be used if thetest is performed carefully and the cli-nician is aware of the limited accuracyof these devices. Rapid measurementmethods available at the bedside in-clude the handheld reflectance color-imeter and electrode methods. Theblood sample is usually obtained froma warmed heel.

Test-strip results demonstrate a rea-sonable correlation with actualplasma glucose concentrations, butthe variation from the actual level maybe as much as 10 to 20 mg/dL.24–27 Un-fortunately, this variation is greatestat low glucose concentrations. There isno point-of-care method that is suffi-ciently reliable and accurate in the lowrange of blood glucose to allow it to beused as the sole method for screeningfor NH.

Because of limitations with “rapid”bedside methods, the blood or plasmaglucose concentration must be con-firmed by laboratory testing orderedstat. A long delay in processing thespecimen can result in a falsely lowconcentration as erythrocytes in thesample metabolize the glucose in theplasma. This problem can be avoidedby transporting the blood in tubes thatcontain a glycolytic inhibitor such asfluoride.

Screening of the at-risk infant for NH andinstitution of prophylactic measures toprevent prolonged or symptomatic NH isa reasonable goal. Treatment of sus-pected NH should not be postponedwhile waiting for laboratory confirma-tion. However, there is no evidence toshow that such rapid treatment will mit-igate neurologic sequelae.

CLINICAL SIGNS

The clinical signs of NH are not specificand include a wide range of local orgeneralized manifestations that arecommon in sick neonates.12,13,17 Thesesigns include jitteriness, cyanosis, sei-zures, apneic episodes, tachypnea,

weak or high-pitched cry, floppiness orlethargy, poor feeding, and eye-rolling.It is important to screen for other pos-sible underlying disorders (eg, infec-tion) as well as hypoglycemia. Suchsigns usually subside quickly with nor-malization of glucose supply andplasma concentration.9,13 Coma andseizures may occur with prolonged NH(plasma or blood glucose concentra-tions lower than 10 mg/dL range) andrepetitive hypoglycemia. The more se-rious signs (eg, seizure activity) usu-ally occur late in severe and pro-tracted cases of hypoglycemia and arenot easily or rapidly reversed with glu-cose replacement and normalizationof plasma glucose concentrations.28–30

Development of clinical signs may beameliorated by the presence of alter-native substrates.31

Because avoidance and treatment ofcerebral energy deficiency is the prin-cipal concern, greatest attentionshould be paid to neurologic signs. Toattribute signs and symptoms to NH,Cornblath et al12 have suggested thatthe Whipple triad be fulfilled: (1) a lowblood glucose concentration; (2) signsconsistent with NH; and (3) resolutionof signs and symptoms after restoringblood glucose concentrations to nor-mal values.12

MANAGEMENT

Any approach tomanagement needs toaccount for the overall metabolic andphysiologic status of the infant andshould not unnecessarily disrupt themother-infant relationship and breast-feeding. The definition of a plasma glu-cose concentration at which interven-tion is indicated needs to be tailored tothe clinical situation and the particularcharacteristics of a given infant. Forexample, further investigation and im-mediate intravenous glucose treat-ment might be instituted for an infantwith clinical signs and a plasma glu-cose concentration of less than 40 mg/

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dL, whereas an at-risk but asymptom-atic term formula-fed infant may onlyrequire an increased frequency offeeding and would receive intravenousglucose only if the glucose values de-creased to less than 25 mg/dL (birth to4 hours of age) or 35 mg/dL (4–24hours of age).32 Follow-up glucose con-centrations and clinical evaluationmust always be obtained to ensurethat postnatal glucose homeostasis isachieved and maintained.

Because severe, prolonged, symptom-atic hypoglycemia may result in neuro-nal injury,27,28,32 prompt intervention isnecessary for infants who manifestclinical signs and symptoms. A reason-able (although arbitrary) cutoff fortreating symptomatic infants is 40mg/dL. This value is higher than the physi-ologic nadir and higher than concen-trations usually associated withclinical signs. A plasma sample for alaboratory glucose determinationneeds to be obtained just before givingan intravenous “minibolus” of glucose(200mg of glucose per kg, 2mL/kg dex-trose 10% in water [D10W], intrave-nously) and/or starting a continuousinfusion of glucose (D10W at 80–100mL/kg per day). A reasonable goal is tomaintain plasma glucose concentra-tions in symptomatic infants between40 and 50 mg/dL.

Figure 1 is a guideline for the screen-ing and management of NH in late-preterm infants and term infants whowere born to mothers with diabetes,small for gestational age, or large forgestational age. In developing a prag-matic approach to the asymptomaticat-risk infant during the first 24 hoursafter birth, mode of feeding, risk fac-tors, and hours of age were consid-ered. This strategy is based on the fol-lowing observations from Cornblathand Ichord13: (1) almost all infants withproven symptomatic NH during thefirst hours of life have plasma glucoseconcentrations lower than 20 to 25

mg/dL; (2) persistent or recurrent NHsyndromes present with equally lowplasma glucose concentrations; and(3) little or no evidence exists to indi-cate that asymptomatic NH at any con-centration of plasma glucose in thefirst days of life results in any adversesequelae in growth or neurologicdevelopment.13

Figure 1 is divided into 2 time periods(birth to 4 hours and 4–12 hours) andaccounts for the changing values ofglucose that occur over the first 12hours after birth. The recommendedvalues for intervention are intended toprovide a margin of safety over con-centrations of glucose associated withclinical signs. The intervention recom-mendations also provide a range ofvalues over which the clinician can de-cide to refeed or provide intravenousglucose. The target glucose concentra-tion is greater than 45 mg/dL beforeeach feeding. At-risk infants should befed by 1 hour of age and screened 30minutes after the feeding. This recom-mendation is consistent with that ofthe World Health Organization. Gavagefeeding may be considered in infantswho are not nippling well. Glucosescreening should continue until 12hours of age for infants born to moth-ers with diabetes and those who arelarge for gestational age and maintainplasma glucose concentrations ofgreater than 40 mg/dL. Late-preterminfants and infants who are small forgestational age require glucose moni-toring for at least 24 hours after birth,because they may be more vulnerableto low glucose concentrations, espe-cially if regular feedings or intrave-nous fluids are not yet established.20 Ifinadequate postnatal glucose ho-meostasis is documented, the clinicianmust be certain that the infant canmaintain normal plasma glucose con-centrations on a routine diet for a rea-sonably extended period (through atleast 3 feed-fast periods) before dis-

charge. It is recommended that the at-risk asymptomatic infant who has glu-cose concentrations of less than 25mg/dL (birth to 4 hours of age) or lessthan 35 mg/dL (4–24 hours of age) berefed and that the glucose value be re-checked 1 hour after refeeding. Subse-quent concentrations lower than 25mg/dL, or lower than 35mg/dL, respec-tively, after attempts to refeed, neces-sitate treatment with intravenous glu-cose. Persistent hypoglycemia can betreated with aminibolus (200mg/kg [2mL/kg] D10W) and/or intravenous infu-sion of D10W at 5 to 8mg/kg perminute,80 to 100 mL/kg per day; the goal is toachieve a plasma glucose concentra-tion of 40 to 50 mg/dL (higher concen-trations will only stimulate further in-sulin secretion). If it is not possible tomaintain blood glucose concentra-tions of greater than 45 mg/dL after 24hours of using this rate of glucose in-fusion, consideration should be givento the possibility of hyperinsulinemichypoglycemia, which is the most com-mon cause of severe persistent hypo-glycemia in the newborn period. Ablood sample should be sent for mea-surement of insulin along with a glu-cose concentration at the time when abedside blood glucose concentrationis less than 40 mg/dL, and an endocri-nologist should be consulted.

SUMMARY

Current evidence does not support aspecific concentration of glucose thatcan discriminate euglycemia from hy-poglycemia or can predict that acuteor chronic irreversible neurologicdamage will result. Therefore, similarto the Canadian Paediatric Societyguidelines, a significantly low concen-tration of glucose in plasma should bereliably established and treated to re-store glucose values to a normal phys-iologic range.5 Recognizing infants atrisk of disturbances in postnatal glu-cose homeostasis and providing amargin of safety by early measures to

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prevent (feeding) and treat (feedingand intravenous glucose infusion) lowconcentrations are primary goals.Follow-up glucose measurements arealways indicated to be sure an infantcan maintain normal glucose concen-trations over several feed-fast cycles.This will also permit recognition of in-fants with persistent hyperinsulinemichypoglycemia and infants with fattyacid oxidation disorders.

LEAD AUTHORDavid H. Adamkin, MD

COMMITTEE ON FETUS AND NEWBORN,2009–2010Lu-Ann Papile, MD, ChairpersonDavid H. Adamkin, MDJill E. Baley, MDVinod K. Bhutani, MDWaldemar A. Carlo, MDPraveen Kumar, MDRichard A. Polin, MDRosemarie C. Tan, MD, PhDKasper S. Wang, MD

Kristi L. Watterberg, MD

LIAISONSCapt Wanda Denise Barfield, MD, MPH –Centers for Disease Control and PreventionWilliam H. Barth Jr, MD – American College ofObstetricians and GynecologistsAnn L. Jefferies, MDRosalie O. Mainous, PhD, RNC, NNP – NationalAssociation of Neonatal NursesTonse N. K. Raju, MD, DCH – National Institutesof Health

STAFFJim Couto, MA

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