Nurse Toni Is Reviewing Manifestations of Newborn Hypoglycemia

Introduction

Neonatal hypoglycemia is a preventable cause of encephalon injury. Information technology is common, affecting 5–15% of all babies (i) and approximately one-half of at-gamble babies (2) and is associated with a range of adverse sequelae (3, 4). However, the optimal frequency and duration of screening, as well as the threshold at which handling would prevent brain injury, remains uncertain. The purpose of this review is to summarize the contempo advances in clinical aspects of transient neonatal hypoglycemia.

Pathophysiology of Neonatal Hypoglycemia

Glucose is the primary metabolic fuel for the fetus. The fetus receives glucose from its female parent through carrier-mediated diffusion downwardly a concentration gradient across the placenta (5, six). Fetal glucose concentrations are ~80% of maternal concentrations and fluctuate with changes in maternal glucose concentrations (seven). The office of insulin in the fetus is as a growth hormone rather than to regulate glucose concentrations, and secretion of insulin occurs at a lower glucose concentration in the fetus than in postnatal life (viii).

Maternal and therefore fetal glucose concentrations increase during labor and delivery in response to secretion of maternal stress hormones such as catecholamines and glucocorticoids (9). Once the umbilical cord is clamped, glucose supply is interrupted and neonatal glucose concentrations subtract, reaching a low indicate ~1–2 h after birth. In turn, insulin secretion decreases while secretion of counter-regulatory hormones such equally glucagon and catecholamines increases, stimulating gluconeogenesis and glycogenolysis, and resulting in a gradual increase in glucose concentrations (9). All the same, these exercise not attain developed concentrations until later on 72 h of age (10, eleven). Delay or pause of this postnatal metabolic accommodation results in neonatal hypoglycemia.

Glucose is an essential metabolic fuel for the brain, and in the newborn the proportionately large brain accounts for almost all of total tissue glucose requirements (12). Thus, low glucose concentrations are likely to event in inadequate brain energy supply. Although the newborn brain can utilize alternative metabolic substrates, the supply of these is limited. Lactate provides a potential alternative fuel in the start 48 h, and ketones may be available on days 3–4, just each can provide only a small proportion of total encephalon energy requirements (13).

Defining Neonatal Hypoglycemia

The definition of neonatal hypoglycemia remains controversial, and has changed over time (14). However, since the major reason for defining hypoglycemia is to place a threshold at which treatment would prevent brain injury, an ideal definition would relate to the glucose concentration at which brain function is compromised. This makes a single definition problematic, as the threshold is probable to vary in different babies, depending amongst other things on gestational historic period, postnatal age, concurrent metabolic demands, co-morbidities and availability of culling metabolic fuels.

The most widely used definition for neonatal hypoglycemia is a glucose concentration of <47 mg/dl (2.6 mmol/l) (15–17). This arises primarily from 2 studies published in 1988, which related glucose concentrations to neurological function. Ane was a retrospective study of 661 preterm babies (birthweight <1,850 m), which reported that a glucose concentration of <47 mg/dl (2.6 mmol/l) on 3 or more than days was associated with an increased risk of developmental delay at eighteen months' corrected age (18). Follow-up of a subgroup showed that reduced motor and arithmetic functioning persisted at eight years (19).

The second study recorded brainstem or somatosensory evoked potentials in 17 infants, of whom only 5 were newborns (twenty). None showed flattening of evoked potentials with a glucose concentration of >47 mg/dl (two.6 mmol/l), although some with a glucose concentration below this still had normal evoked potentials. Both studies concluded that a glucose concentration of >47 mg/dl (2.6 mmol/l) was likely to be safe.

In situations where show-based decisions are not possible, operational thresholds offer a businesslike guide to clinicians for when intervention may be warranted (ane). Screening protocols have recommended different operational thresholds ranging from 18 to 60 mg/dl (one.0–iii.3 mmol/50) (21–24). However, almost recommend aiming for a minimum glucose concentration shut to 47 mg/dl (ii.6 mmol/50) in late preterm and term babies more than than a few hours old or requiring treatment.

Incidence and Risk Factors

The incidence of neonatal hypoglycemia varies between studies depending on the diagnostic threshold, the glucose screening protocol and measurement method used, and the population studied (25). All the same, the incidence of transient neonatal hypoglycemia is estimated to be 5–fifteen% of newborns (1, 26), and in at-adventure babies, it approximates l% (two) (Table i). Babies with multiple risk factors do non accept a higher incidence merely may experience more severe hypoglycemia.

Table 1. Take chances factors for neonatal hypoglycemia.

Management of Neonatal Hypoglycemia

Screening for Neonatal Hypoglycemia

The clinical signs of neonatal hypoglycemia include, but are not limited to, cyanosis, apnea, altered level of consciousness, seizures, lethargy, and poor feeding (24). However, since many of these signs are non-specific, and the bulk of babies with low glucose concentrations show no clinical signs, information technology is recommended that all babies with hazard factors undergo regular glucose monitoring.

The optimal frequency and duration of screening remain uncertain. Most protocols recommend screening inside 1–four h after nativity and and so every 3 or 4 h until euglycemia is maintained over two or iii consecutive glucose measurements (15, 21, 22, 24). Nonetheless, all of these guidelines are informed by expert stance and lack a reliable prove base (28).

Some specify different monitoring periods dependent on the clinical profile of the baby. For instance, the American University of Pediatrics recommends that monitoring continues until 12 h afterward birth for infants of diabetic mothers or large for gestational age, but for 24 h for babies who are born late preterm or small for gestational age (21). However, there is no evidence to suggest that cognitive glucose requirements vary between at-risk groups (15).

One report that screened at-risk babies using an authentic glucose oxidase method one–2 h later on birth then every 3–iv h before feeds for the showtime 24 h and every 3–viii h from 24 to 48 h reported no difference between risk groups in the incidence or severity of neonatal hypoglycemia, suggesting that a single screening protocol would be reasonable for all babies at chance (2).

Blood Glucose Monitoring

Intermittent Glucose Monitoring

A common method for measuring glucose concentrations in neonates is by heel-prick blood sampling analyzed using point-of-intendance non-enzymatic glucometers. These provide quick results at a low price, are readily available in neonatal units, user-friendly and require pocket-size volumes of blood (29).

Nevertheless, these devices are designed for monitoring loftier glucose concentrations in diabetics, and are affected by several factors that vary widely in newborns including bilirubin concentrations and hematocrit. They are inaccurate at low glucose concentrations, with estimated false positive and false negative rates of ten–30%, and are not recommended as the sole method for diagnosis of neonatal hypoglycemia (21, xxx). If point-of-intendance non-enzymatic glucometers are used for screening, it is critical to confirm the results with a laboratory method (21), just best practice is to use more than accurate methods from the outset.

Laboratory methods employ enzymatic reactions including glucose oxidase, hexokinase or dehydrogenase (29) which are more than accurate and sensitive for detecting neonatal hypoglycemia (31, 32). However, laboratory methods are costly, take time which can filibuster prompt intervention, and accuracy is also reliant on the quality of the plasma sample (29). More than recent guidelines recommend claret gas analyzers which are quick and accurate if they are immediately available (xv, 24).

A more than feasible alternative in many settings is the newer enzymatic point-of-intendance analyzers, which have the same accurateness every bit laboratory methods but the convenience and speed of a cot-side measurement. Although they are more expensive per test than the widely used (but inaccurate) test strip glucometers, a contempo cost analysis ended that enzymatic glucometers incurred lower direct costs overall because they avoided the additional costs of retesting in the laboratory (33).

Continuous Interstitial Glucose Monitoring

Continuous interstitial glucose monitors contain a sensor placed under the skin, and a recording device, often remote from the sensor, which converts the electrical current generated in the sensor to a glucose concentration using an inbuilt algorithm. Virtually devices provide a reading every five min, giving detailed information most glycemic control including the duration, frequency, and severity of hypoglycemia (34).

Continuous glucose monitors take several limitations. They require calibration against blood glucose concentrations at least every 12 h, so they exercise not abolish the need for blood tests, and more frequent scale is recommended for greater accuracy and precision (35). Continuous glucose monitors are too prone to measurement error, and the reading can drift from the calibrated value without detection (35). Because, like point-of-intendance glucometers, they are designed for apply in diabetes, they are less accurate at depression glucose concentrations. The lag catamenia between changes in blood glucose concentrations and changes in the continuous monitor reading is unknown simply could be up to thirty min or more, due both to the time required for glucose to diffuse from blood to interstitial fluid, and to delays congenital into the algorithms, so that the rapid changes in glucose concentrations that are common in newborn babies are poorly reported by continuous monitors (36, 37). Infection at the site of sensor insertion is a theoretical concern, merely in exercise has rarely been reported, and most studies have reported that sensors tin be left in place for a calendar week without complications, even in very low birthweight babies (38).

Most chiefly, in that location is a lack of bear witness on whether continuous glucose monitoring is associated with clinical benefits or harms. Continuous glucose monitoring detects many more episodes of low glucose concentrations than does intermittent blood glucose measurement. For example, in 102 babies at risk of hypoglycemia, continuous glucose monitoring identified 11% more babies and l% more episodes of low glucose than intermittent glucose monitoring (39). Others accept reported like differences (38, 40). Thus, there is a risk that continuous glucose monitoring may lead to a big increment in diagnosis and treatment, but without evidence that these additional detected episodes are related to brain injury, or that additional treatment volition take whatever long-term benefit.

Despite these limitations, continuous glucose monitoring has enormous potential to ameliorate the management of neonatal hypoglycemia. A randomized trial in 48 very low birthweight babies showed that utilise of continuous glucose monitoring reduced the number of blood samples taken, detected more episodes of neonatal hypoglycemia and reduced the duration of an episode by half when compared with intermittent glucose monitoring (40). Some other randomized trial in 50 very preterm babes reported that continuous glucose monitoring in conjunction with an algorithm for glucose infusion titration reduced the duration and severity of hypoglycemic episodes, thereby promoting glycemic stability (41). All the same, it is not even so known if this improved stability will lead to improved later outcomes.

Treating Neonatal Hypoglycemia

The goal of treating neonatal hypoglycemia is to prevent or minimize brain injury by maintaining a glucose concentration in a higher place an acceptable threshold (25). The usual initial approach is to feed the baby, using either formula or breast milk. When glucose concentrations are <18–25 mg/dl (1.0–i.iv mmol/l) intravenous dextrose (bolus 200 mg/kg followed by an infusion of effectually iv–8 mg/kg per infinitesimal) is usually required (21, 24). However, administering intravenous dextrose involves admission to the neonatal intensive care unit (NICU), which is plush, invasive, and separates the mother from her baby, which in turn can increment maternal anxiety and interfere with the establishment of breastfeeding. Severe or prolonged hypoglycemia, indicated by persistently high or ongoing (≥3 days) intravenous glucose requirements, suggest underlying endocrine or metabolic pathology and further investigation is required (Table one). Elevated insulin concentrations bespeak hyperinsulinism, which suppresses the product of alternative metabolic fuels, and hence maintaining blood glucose ≥ iii.5 mmol/l is recommended (24). Additional treatments, such as diazoxide (42), glucagon (24, 43) or glucocorticoids (44) may be required.

Oral dextrose gel 200 mg/kg (0.5 ml/kg of xl% dextrose), in combination with feeding, is increasingly recommended equally a get-go-line treatment for asymptomatic neonatal hypoglycemia (45, 46). A randomized trial of 237 tardily preterm and term babies at risk of neonatal hypoglycemia [ <47 mg/dl (2.half dozen mmol/l)] demonstrated that compared with feeding alone, 40% oral dextrose gel 200 mg/kg plus feeding resulted in fewer treatment failures (hypoglycemia after ii treatment attempts), reduced admission to NICU for hypoglycemia and reduced formula feeding at ii weeks of age (47). A 2-yr follow-upward established safe past demonstrating similar rates of processing difficulty and neurosensory impairment between the oral dextrose and placebo groups (48). A subsequent cost-utility analysis ended that dextrose gel resulted in a cost-saving of US$782 per babe (49).

The incorporation of oral dextrose gel into clinical practice has been evaluated in pre-and mail-introduction observational studies in several parts of the earth, with most reporting that oral dextrose was associated with a reduced NICU admission and increased breastfeeding (fifty–54). Its use is now recommended in several national guidelines (xv, 22, 24).

Prophylaxis

There is some prove that fifty-fifty transient and undetected episodes of neonatal hypoglycemia may exist associated with adverse sequelae. One written report of ane,395 babies born in a center where glucose screening was universal showed that a single episode of transient neonatal hypoglycemia [ <35 mg/dl (1.nine mmol/l)] was associated with lower 4th-grade literacy and numeracy proficiency at 10 years of historic period (55). The Children With Hypoglycemia and Their After Evolution (CHYLD) study demonstrated that clinically undetected low interstitial glucose concentrations were associated with an increased hazard of executive dysfunction at 4.5 years of historic period (56). These findings suggest that even an effective treatment for neonatal hypoglycemia would non be sufficient to optimize outcomes for all babies, and prophylaxis needs to be considered.

The prophylactic measures currently recommended include early feeding, ensuring babies are warm and dry, and early pare-to-peel contact (57). These measures are thought to have a glucose sparing effect (58), merely the evidence that they change blood glucose concentrations or the incidence of hypoglycemia is limited (59–61).

Oral dextrose gel is being tested as an additional safety measure to prevent hypoglycemia in at-run a risk babies. A dose-finding trial (Pre-hPOD) of 416 at-take chances babies randomized to either placebo or dextrose gel at one of four dissimilar dosing schedules reported that a single dose of prophylactic oral forty% dextrose gel (200 mg/kg) in combination with breastfeeding was the about effective and practical dose (62), with a number needed to treat to forestall i case of hypoglycemia of 10. Farther, the treatment was institute to be acceptable, well tolerated, and had no adverse events (62). Follow-upward at two years' corrected age showed no agin effects, similar rates of neurosensory impairment betwixt the groups, and a trend toward improved executive role scores in the dextrose gel group (63).

A quasi-experimental written report of 236 at-risk babies reported that compared with feeding, condom oral dextrose gel 200 mg/kg was not associated with a decreased incidence of hypoglycemia [ <40 mg/dl (ii.two mmol/fifty)] or access to NICU (64). Still, this study was not randomized, and the preparation used (Insta-Glucose gel) includes additional carbohydrates other than dextrose, which are likely to have competed with dextrose for membrane uptake and potentially reduced the effectiveness of this arroyo.

A multicenter randomized trial (hPOD) investigating whether prophylactic oral dextrose gel prevents neonatal hypoglycemia and hence reduces NICU admission has finished recruitment (ANZC Trials Registry – ACTRN12614001263684) (65). The results, and particularly the findings of the planned long-term follow-upwardly, will provide valuable insight into whether prophylaxis with dextrose gel should exist introduced into clinical do.

Outcomes of Neonatal Hypoglycemia

Magnetic Resonance Imaging (MRI) studies have shown that neonatal hypoglycemia can cause brain injury (66, 67). The well-nigh widely reported pattern of acute brain injury is localized in the parietal and occipital regions (68), which are involved in visual processing. Yet, the show is inconsistent on whether neonatal hypoglycemia is associated with later visual problems (69). Injury may extend beyond these regions with reports of global or periventricular damage (67) as well every bit damage to the basal ganglia and thalamic regions (67, 70).

A systematic review and meta-analysis of six cohort studies with a sample size of ane,675 babies reported that neonatal hypoglycemia [definitions ranged from <20–47 mg/dl (1.i–2.6 mmol/fifty)] was not associated with neurodevelopmental damage, cognitive or motor deficits between 2 and 5 years of age (iv). However, neonatal hypoglycemia was associated with a iii-fold increased take a chance of visual-motor impairment and executive dysfunction at four years of age. These risks were heightened for children who had experienced severe, recurrent or clinically undetected neonatal hypoglycemia (56). In older children, limited data (two studies, sample size of 54 babies) showed that neonatal hypoglycemia was associated with more than a 3-fold increased take chances of neurodevelopmental impairment at six–eleven years of age, and a 2-fold increase in depression numeracy and literacy (4). No studies reported on outcomes for adolescents.

Most of the evidence about long-term outcomes later on neonatal hypoglycemia comes from retrospective observational studies, few of which take controlled for potential confounders or looked at outcomes beyond very early childhood. For instance, infants of mothers with diabetes, who are at increased risk of neonatal hypoglycemia, accept an increased risk of adverse outcomes (71, 72), but it is unclear how much of this risk is owing to neonatal hypoglycemia. There is high heterogeneity between the studies which made comparing outcomes problematic, and there have been frequent calls for robust randomized trial testify (iii).

A randomized non-inferiority trial was the first to brainstorm to address this major knowledge gap by comparing handling at a threshold of 47 mg/dl (2.6 mmol/l) against treatment at a lower threshold of 36 mg/dl (two.0 mmol/fifty) among a sample of 689 otherwise healthy tardily preterm and term babies with mild-moderate hypoglycemia [36 mg/dl (ii.0 mmol/l)−46 mg/dl (2.5 mmol/50)] (73). Babies with early (birth to 2 h) and astringent [ ≤ 35 mg/dl (1.9 mmol/50)] hypoglycemia were excluded. In babies randomized to treatment at the lower threshold, fewer were monitored and treated, but at that place were more than astringent and recurrent hypoglycemic episodes (≥4 episodes) compared with babies in the higher threshold grouping. Infirmary costs and duration of stay were similar between the groups, as were motor and cerebral performance at 18 months on the Bayley Scales for Babe and Toddler Evolution. Still, since previous studies have shown no human relationship betwixt neonatal hypoglycemia and motor or cognitive office at this age (4), this finding is not surprising, and the greater exposure to astringent and recurrent hypoglycemia in the low threshold grouping is of concern. Much longer follow-upwards, at least to schoolhouse age, volition be essential to realize the true value of this important written report.

Determination

Over the last few years, neonatal hypoglycemia has received much attention. Yet, what remains unclear is the extent to which transient asymptomatic neonatal hypoglycemia is associated with brain injury and neurodevelopmental damage, and if then, at what glucose concentration maintained for how long. To address this, adequately powered randomized trials are needed of both prophylactic and treatment interventions at different glucose thresholds, with neurodevelopmental outcomes assessed at to the lowest degree to school age.

Author Contributions

TE and JH contributed to the literature search and the pattern of the review. TE wrote the starting time draft of the manuscript and contributed to further revisions. JH contributed to the writing of the manuscript and supervised the study. Both authors contributed to the article and approved the submitted version.

Funding

This research was supported in part by grants from The Health Research Council of New Zealand (13/131, xv/216, 17/240) and the Eunice Kennedy Shriver National Establish of Child Health and Homo Development (R01HD069622, 1RO1HD091075).

Disclaimer

The content is solely the responsibility of the authors and does not necessarily represent the official views of the Eunice Kennedy Shriver National Institute of Child Wellness and Man Development or the National Institutes of Health.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could exist construed as a potential conflict of interest.

References

1. Hay WW, Raju TNK, Higgins RD, Kalhan SC, Devaskar SU. Knowledge gaps and research needs for understanding and treating neonatal hypoglycemia: workshop report from Eunice Kennedy Shriver National Institute of Child Health and Human Development. J Pediatr. (2009) 155:612–vii. doi: ten.1016/j.jpeds.2009.06.044

CrossRef Full Text | Google Scholar

three. Boluyt Due north, van Kempen A, Offringa One thousand. Neurodevelopment after neonatal hypoglycemia: a systematic review and design of an optimal future written report. Pediatrics. (2006) 117:2231–43. doi: ten.1542/peds.2005-1919

PubMed Abstract | CrossRef Full Text | Google Scholar

4. Shah R, Harding JE, Brown J, McKinlay C. Neonatal glycaemia and neurodevelopmental outcomes: a systematic review and meta-analysis. Neonatology. (2019) 115:116–26. doi: 10.1159/000492859

PubMed Abstract | CrossRef Full Text | Google Scholar

7. Bozzetti P, Ferrari MM, Marconi AM, Ferrazzi E, Pardi K, Makowski EL, et al. The relationship of maternal and fetal glucose concentrations in the human from midgestation until term. Metabolism. (1988) 37:358–63. doi: 10.1016/0026-0495(88)90136-ix

PubMed Abstract | CrossRef Total Text | Google Scholar

x. Srinivasan M, Pildes RS, Cattamanchi Chiliad, Voora South, Lilien LD. Plasma glucose values in normal neonates: a new look. J Pediatr. (1986) 109:114–vii. doi: 10.1016/S0022-3476(86)80588-1

PubMed Abstract | CrossRef Full Text | Google Scholar

11. Harris D, Weston PJ, Gamble GD, Harding JE. Glucose profiles in healthy term infants in the first five days: the Glucose in Well Babies (GLOW) Study. J Pediatr. (2020) 223:34–41e.4. doi: ten.1016/j.jpeds.2020.02.079

PubMed Abstruse | CrossRef Total Text | Google Scholar

13. Harris D, Weston PJ, Harding JE. Lactate, rather than ketones, may provide alternative cognitive fuel in hypoglycaemic newborns. Arch Dis Child Fetal Neonatal Ed. (2015) 100:F161–iv. doi: 10.1136/archdischild-2014-306435

PubMed Abstract | CrossRef Full Text | Google Scholar

sixteen. Dixon KC, Ferris RL, Marikar D, Chong Yard, Mittal A, Manikam Fifty, et al. Definition and monitoring of neonatal hypoglycaemia: a nationwide survey of NHS England Neonatal Units. Arch Dis Kid Fetal Neonatal Ed. (2017) 102:F92–3. doi: 10.1136/archdischild-2016-311473

PubMed Abstract | CrossRef Full Text | Google Scholar

17. Harris D, Weston PJ, Battin MR, Harding JE. A survey of the management of neonatal hypoglycaemia inside the Australian and New Zealand Neonatal Network. J Paediatr Child Wellness. (2014) 50:E55–62. doi: 10.1111/j.1440-1754.2009.01599.x

PubMed Abstract | CrossRef Full Text | Google Scholar

23. Cornblath M, Hawdon JM, Williams AF, Aynsley-Light-green A, Ward-Platt MP, Schwartz R, et al. Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds. Pediatrics. (2000) 105:1141–5. doi: 10.1542/peds.105.5.1141

PubMed Abstract | CrossRef Full Text | Google Scholar

25. Harding JE, Harris D, Hegarty JE, Alsweiler JM, McKinlay CJD. An emerging evidence base of operations for the management of neonatal hypoglycaemia. Early Hum Dev. (2017) 104:51–6. doi: 10.1016/j.earlhumdev.2016.12.009

PubMed Abstract | CrossRef Total Text | Google Scholar

26. Bromiker R, Perry A, Kasirer Y, Einav S, Klinger G, Levy-Khademi F. Early neonatal hypoglycemia: incidence of and risk factors. A accomplice written report using universal betoken of intendance screening. J Matern Neonatal Med. (2019) 32:786–92. doi: 10.1080/14767058.2017.1391781

PubMed Abstract | CrossRef Full Text | Google Scholar

27. Thornton PS, Stanley CA, De Leon DD, Harris D, Haymond MW, Hussain Thou, et al. Recommendations from the Pediatric Endocrine Society for evaluation and management of persistent hypoglycemia in neonates, infants, and children. J Pediatr. (2015) 167:238–45. doi: 10.1016/j.jpeds.2015.03.057

PubMed Abstract | CrossRef Full Text | Google Scholar

28. Adamkin DH. Neonatal hypoglycemia. In: Martin G, Rosenfield West, editors. Common Problems in the Newborn Plant nursery. An Evidence Case-Based Guide. Basel: Springer (2019). p. 99–108.

Google Scholar

31. Sreenivasa B, Kumar K 5, Sreenivasa B. Comparative study of blood glucose levels in neonates using glucometer and laboratory glucose oxidase method. Curr Pediatr Res. (2015) 19:29–32.

Google Scholar

32. Khan AI, Vasquez Y, Gray J, Wians Jr FH, Kroll MH. The variability of results between point-of-care testing glucose meters and the central laboratory analyzer. Curvation Pathol Lab Med. (2006) 130:1527–32. doi: 10.1043/1543-2165(2006)1301527:TVORBP2.0.CO

PubMed Abstract | CrossRef Total Text | Google Scholar

34. McKinlay CJD, Chase JG, Dickson J, Harris D, Alsweiler JM, Harding JE. Continuous glucose monitoring in neonates: a review. Matern Heal Neonatol Perinatol. (2017) iii:i–9. doi: 10.1186/s40748-017-0055-z

PubMed Abstract | CrossRef Total Text | Google Scholar

35. Point M, Le Compte A, Harris D, Weston PJ, Harding JE. Impact of retrospective scale algorithms on hypoglycemia detection in newborn infants using continuous glucose monitoring. Diabetes Technol Ther. (2012) 14:883–90. doi: ten.1089/dia.2012.0111

PubMed Abstruse | CrossRef Full Text | Google Scholar

37. Harris D, Battin MR, Williams CE, Weston PJ, Harding JE. Cot-side electro-encephalography and interstitial glucose monitoring during insulin-induced hypoglycaemia in newborn lambs. Neonatology. (2009) 95:271–8. doi: ten.1159/000166847

PubMed Abstract | CrossRef Total Text | Google Scholar

38. Beardsall K, Ogilvy-Stuart AL, Ahluwalia J, Thompson 1000, Dunger DB. The continuous glucose monitoring sensor in neonatal intensive intendance. Arch Dis Kid Fetal Neonatal Ed. (2005) 90:F307–10. doi: 10.1136/adc.2004.051979

PubMed Abstract | CrossRef Total Text | Google Scholar

39. Harris D, Battin MR, Weston PJ, Harding JE. Continuous glucose monitoring in newborn babies at take a chance of hypoglycemia. J Pediatr. (2010) 157:198–202. doi: 10.1016/j.jpeds.2010.02.003

PubMed Abstract | CrossRef Full Text | Google Scholar

twoscore. Uettwiller F, Chemin A, Bonnemaison East, Favrais M, Saliba E, Labarthe F. Real-fourth dimension continuous glucose monitoring reduces the duration of hypoglycemia episodes: a randomized trial in very low birth weight neonates. PLoS ONE. (2015) 10:e0116255. doi: 10.1371/journal.pone.0116255

PubMed Abstract | CrossRef Full Text | Google Scholar

41. Galderisi A, Facchinetti A, Steil GM, Ortiz-Rubio P, Cavallin F, Tamborlane WV, et al. Continuous glucose monitoring in very preterm infants: a randomized controlled trial. Pediatrics. (2017) 140:1–ten. doi: 10.1542/peds.2017-1162

PubMed Abstract | CrossRef Full Text | Google Scholar

42. Hoe FM, Thornton PS, Wanner LA, Steinkrauss L, Simmons RA, Stanley CA. Clinical features and insulin regulation in infants with a syndrome of prolonged neonatal hyperinsulinism. J Pediatr. (2006) 148:207–12. doi: 10.1016/j.jpeds.2005.10.002

PubMed Abstract | CrossRef Full Text | Google Scholar

43. Miralles RE, Lodha A, Perlman Yard, Moore AM. Experience with intravenous glucagon infusions equally a treatment for resistant neonatal hypoglycemia. Curvation Pediatr Adolesc Med. (2002) 156:999–1004. doi: 10.1001/archpedi.156.10.999

PubMed Abstract | CrossRef Full Text | Google Scholar

46. Weston PJ, Harris D, Battin M, Brownish J, Hegarty JE, Harding JE. Oral dextrose gel for the treatment of hypoglycaemia in newborn infants. Cochrane Database Syst Rev. (2016) CD011027. doi: x.1002/14651858.CD011027.pub2

PubMed Abstract | CrossRef Total Text | Google Scholar

47. Harris D, Weston PJ, Bespeak M, Chase JG, Harding JE. Dextrose gel for neonatal hypoglycaemia (the Sugar Babies Written report): a randomised, double-blind, placebo-controlled trial. Lancet. (2013) 382:2077–83. doi: 10.1016/S0140-6736(13)61645-ane

PubMed Abstruse | CrossRef Full Text | Google Scholar

48. Harris D, Alsweiler JM, Ansell JM, Take a chance GD, Thompson B, Wouldes TA, et al. Event at ii years after dextrose gel treatment for neonatal hypoglycaemia: follow-upwardly of a randomized trial. J Pediatr. (2016) 170:54–9. doi: x.1016/j.jpeds.2015.10.066

PubMed Abstract | CrossRef Full Text | Google Scholar

49. Glasgow MJ, Harding JE, Edlin R, Alsweiler JM, Hunt JG, Harris D, et al. Cost assay of treating neonatal hypoglycemia with dextrose gel. J Pediatr. (2018) 198:151–5.e1. doi: x.1016/j.jpeds.2018.02.036

PubMed Abstract | CrossRef Total Text | Google Scholar

50. Gregory Yard, Turner D, Benjamin CN, Monthe-Dreze C, Johnson L, Hurwitz S, et al. Incorporating dextrose gel and feeding in the treatment of neonatal hypoglycaemia. Arch Dis Child Fetal Neonatal Ed. (2020) 105:45–9. doi: x.1136/archdischild-2018-316430

PubMed Abstruse | CrossRef Full Text | Google Scholar

51. Rawat M, Chandrasekharan P, Turkovich Southward, Barclay North, Perry K, Schroeder East, et al. Oral dextrose gel reduces the need for intravenous dextrose therapy in neonatal hypoglycemia. Biomed Hub. (2016) 1:1–nine. doi: 10.1159/000448511

PubMed Abstruse | CrossRef Total Text | Google Scholar

52. Bennett C, Fagan E, Chaharbakhshi East, Zamfirova I, Flicker J. Implementing a protocol using glucose gel to care for neonatal hypoglycemia. Nurs Womens Wellness. (2016) 20:64–74. doi: 10.1016/j.nwh.2015.11.001

PubMed Abstruse | CrossRef Full Text | Google Scholar

53. Makker K, Alissa R, Dudek C, Travers Fifty, Smotherman C, Hudak ML. Glucose gel in infants at chance for transitional neonatal hypoglycemia. Am J Perinatol. (2018) 35:1050–six. doi: ten.1055/due south-0038-1639338

PubMed Abstract | CrossRef Full Text | Google Scholar

54. Stewart CE, Sage ELM, Reynolds P. Supporting 'baby friendly': a quality improvement initiative for the management of transitional neonatal hypoglycaemia. Arch Dis Kid Fetal Neonatal Ed. (2016) 101:F344–vii. doi: x.1136/archdischild-2015-308950

PubMed Abstruse | CrossRef Full Text | Google Scholar

55. Kaiser JR, Bai S, Gibson Northward, The netherlands Grand, Lin TM, Swearingen CJ, et al. Clan betwixt transient newborn hypoglycemia and 4th-grade achievement test proficiency: a population-based study. JAMA Pediatr. (2015) 169:913–21. doi: ten.1001/jamapediatrics.2015.1631

CrossRef Full Text | Google Scholar

56. McKinlay CJD, Alsweiler JM, Anstice NS, Burakevych N, Chakraborty A, Hunt JG, et al. Clan of neonatal glycemia with neurodevelopmental outcomes at iv.5 years. JAMA Pediatr. (2017) 171:972–83. doi: 10.1001/jamapediatrics.2017.1579

CrossRef Full Text | Google Scholar

58. Moore ER, Bergman North, Anderson GC, Medley Northward. Early skin-to-skin contact for mothers and their healthy newborn infants. Cochrane Database Syst Rev. (2016). doi: ten.1002/14651858.CD003519.pub4

CrossRef Full Text | Google Scholar

59. Sugariness DG, Hadden D, Halliday HL. The outcome of early feeding on the neonatal blood glucose level at one-hour of age. Early on Hum Dev. (1999) 55:63–half dozen. doi: x.1016/S0378-3782(99)00004-3

PubMed Abstruse | CrossRef Total Text | Google Scholar

lx. Chiruvolu A, Miklis KK, Stanzo KC, Petrey B, Groves CG, McCord Thousand, et al. Effects of peel-to-skin care on belatedly preterm and term infants at-gamble for neonatal hypoglycemia. Pediatr Qual Saf. (2017) ii:1–vii. doi: 10.1097/pq9.0000000000000030

PubMed Abstruse | CrossRef Full Text | Google Scholar

61. Chertok IR, Raz I, Shoham I, Haddad H, Wiznitzer A. Furnishings of early on breastfeeding on neonatal glucose levels of term infants built-in to women with gestational diabetes. J Hum Nutr Diet. (2009) 22:166–9. doi: x.1111/j.1365-277X.2008.00921.10

PubMed Abstract | CrossRef Full Text | Google Scholar

62. Hegarty JE, Harding JE, Gamble GD, Crowther CA, Edlin R, Alsweiler JM. Prophylactic oral dextrose gel for newborn babies at risk of neonatal hypoglycaemia: a randomised controlled dose-finding trial (the Pre-hPOD Study). PLoS Med. (2016) thirteen:e1002155. doi: x.1371/journal.pmed.1002155

PubMed Abstruse | CrossRef Total Text | Google Scholar

63. Griffith R, Hegarty JE, Alsweiler JM, Adventure GD, May R, McKinlay CJD, et al. Two-year outcomes after dextrose gel prophylaxis for neonatal hypoglycaemia. Arch Dis Childh Fetal Neonatal Ed. (2020). doi: 10.1136/archdischild-2020-320305. [Epub ahead of print].

PubMed Abstruse | CrossRef Total Text | Google Scholar

64. Coors SM, Cousin JJ, Hagan JL, Kaiser JR. Safety dextrose gel does non prevent neonatal hypoglycemia: a quasi-experimental pilot study. J Pediatr. (2018) 198:156–61. doi: 10.1016/j.jpeds.2018.02.025

PubMed Abstruse | CrossRef Total Text | Google Scholar

65. Harding JE, Hegarty JE, Crowther CA, Edlin R, Gamble G, Alsweiler JM. Randomised trial of neonatal hypoglycaemia prevention with oral dextrose gel (hPOD): written report protocol. BMC Pediatr. (2015) 15:1–5. doi: 10.1186/s12887-015-0440-6

PubMed Abstract | CrossRef Full Text | Google Scholar

67. Burns CM, Rutherford MA, Boardman JP, Cowan FM. Patterns of cognitive injury and neurodevelopmental outcomes afterward symptomatic neonatal hypoglycemia. Pediatrics. (2008) 122:65–74. doi: x.1542/peds.2007-2822

PubMed Abstract | CrossRef Total Text | Google Scholar

68. Alkalay AL, Flores-Sarnat 50, Sarnat HB, Moser FG, Simmons CF. Encephalon imaging findings in neonatal hypoglycemia: case report and review of 23 cases. Clin Pediatr. (2005) 44:783–90. doi: x.1177/000992280504400906

PubMed Abstract | CrossRef Full Text | Google Scholar

69. Paudel N, Chakraborty A, Anstice N, Jacobs RJ, Hegarty JjE, Harding JE, et al. Neonatal hypoglycaemia and visual development: a review. Neonatology. (2017) 112:47–52. doi: x.1159/000456705

PubMed Abstract | CrossRef Total Text | Google Scholar

70. Gataullina S, Lonlay PDE, Dellatolas M, Valayannapoulos V, Napuri S, Damaj L, et al. Topography of brain damage in metabolic hypoglycaemia is determined by age at which hypoglycaemia occurred. Dev Med Kid Neurol. (2013) 55:162–6. doi: ten.1111/dmcn.12045

PubMed Abstract | CrossRef Full Text | Google Scholar

71. Lin C-H, Lin W-D, Chou IC, Lee I-C, Hong Due south-Y. Infants of mothers with diabetes and subsequent attention arrears hyperactivity disorder: a retrospective cohort study. Front Pediatr. (2019) vii:i–7. doi: 10.3389/fped.2019.00452

PubMed Abstruse | CrossRef Full Text | Google Scholar

72. Pacaud D, Dewey D. Neurocognitive event of children exposed to severe hypoglycemia in utero. Diabetes Manag. (2011) ane:129–xl. doi: ten.2217/dmt.ten.10

CrossRef Full Text | Google Scholar

73. van Kempen AA, Eskes PF, Nuytemans DHGM, van der Lee JH, Dijksman LM, van Veenendaal NR, et al. Lower versus traditional treatment threshold for neonatal hypoglycemia. North Engl J Med. (2020) 382:534–44. doi: 10.1056/NEJMoa1905593

PubMed Abstract | CrossRef Full Text | Google Scholar

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Source: https://www.frontiersin.org/articles/10.3389/fped.2020.562251/full

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