Kulvinder Kochar Kaur*

Scientific Director, Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India

*Corresponding Author: Kulvinder Kochar Kaur, Scientific Director, Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India.

Received: April 26, 2021; Published: July 08, 2021

Citation: Kulvinder Kochar Kaur. “Significance of Strategies to Avoid Neonatal Hypoglycemia in Both Transient and Persistent and Management and Prophylaxis to Avoid Long Term Sequelae”. Acta Scientific Paediatrics 4.8 (2021): 33-34.

Introduction

Neonatal hypoglycemia [NH]-avoidable cause of brain injury, common-influences 5 - 15% babies and 50% of at risk babies-linked with range of side effects [1]. Ideal time of screening, threshold at which treatment avoids brain damage not clear. Glucose primary metabolic fuel for fetus. Glucose got from mother via carrier-modulated diffusion down a concentration gradient via the placenta [2]. Fetal glucose amounts 80% of maternal amounts vary with alterations in maternal glucose amounts. In fetus function of insulin is like GH instead of controlling glucose amounts and liberation of insulin-takes place at lower insulin in fetus as compared to postnatal life [3].

Pathophysiology-Maternal and thus fetal glucose amounts escalate at labour time and delivery- secondary to liberation of maternal stress hormones-like catecholamines and glucocorticoid [4]. Tying umbilical cord glucose amounts supply interrupted reduction in glucose amounts in neonatal glucose low peak decreased -low point of glucose amounts reached 1 - 2hr following birth insulin liberation decreases and counter controlling hormones-glucagon and catecholamines escalate-------) stmn of gluconeogenesis and glycogenolysis gradual escalation of glucose amounts but don’t reach adult amounts till 72h age [5]. Delay of postnatal adaptation NH. Glucose-Necessary fuel-brain and in newborn proportionately large brain explains total tissue needs [6]. Hence low glucose amounts not enough brain energy provision. Though can use alternative metabolic substrates limited supply. Lactate serves as alternative fuel, but in 1^st 48h, ketones probably on d3-4 although each very little total brain energy demands met. At risk factors (for transient NH-preterm birth, SGA. LFD, Infant of DM mother, perinatal stress (birth asphyxia, hypothermia, resp distress, sepsis, poor feeding) [For continuous NH-Congenital hyperinsulinism, hypopituitarism, (ACTH deficiency, GH deficiency), Cortisol deficiency, Glycogen storage dis, gluconeogenesis disorder (FBP deficiency, PEPCK deficiency, PC deficiency, FA oxidative defects definition contradictory major goal find a threshold avoids brain damage. Commonest used is glucose amounts < 47 mg/dl [2.6 mmol/l) [7,8] main source 2 studies-66 preterm babies (BW < 1850 gm) -- glucose amounts -- < 47 mg/dl [2.6 mmol/l) [on 3 or ≥ 3 with enhanced risk of developmental delay at 18 month [6]. Follow Up-decreased motor &mathematical function continued till 8yrs [6]. 2^nd study recorded brain stem or somatosensory evoked potentials in 17 infants 5 were newborn [6]. Neither demonstrated flattening of evoked potentials with glucose a amounts > 47 mg/dl [2.6 mmol/l), despite some with glucose a amounts -- < 47 mg/dl [2.6 mmol/l) [also possessed normal evoked potentials-both conclusions glucose amounts > 47 mg/dl [2.6 mmol/l) safe amounts incidence risk factors incidence differs study type, diagnostic threshold glucose screening method-but incidence of transient NH 5 - 15% of newborns [9], in at risk newborns-50%-Babies with a lot of factors might not have >incidence but gave robust hypoglycemia.

Management Screening Clinical signs-cyanosis, apnea, changed consciousness levels, convulsions, poor feeding [6] not only these many nonspecific most babies with low a amounts no clinical signs-advocate all babies with at risk factors regular screening of glucose-maximum advocate 1 - 4h following birth and then 3 or 4h till euglycemia sustained over 2 - 3 consecutive glucose amounts American Academy of Paediatrics (AAP) - advocate continuous monitoring till 12h following birth for diabetic mothers and large for date (LFD) babies for 24h late preterm or small for gestational age (SGA) [6]. No proof to point cerebral glucose amounts differ in at risk groups [6]. Blood glucose amounts monitor, various methods [6]. Continuous interstitial glucose amounts monitor-tedious [6]. Treatment of NH-Goal-avoid or minimize brain damage-sustain glucose amounts above acceptable threshold. Initially usually feed baby with formula feed/breast feed if glucose amounts < 18 - 25 mg/dl (1 - 1.4 mmol/l) iv dextrose (bolus 200 mg/kg followed by infusion of approximately 4 - 8 mg/kg/min-usually needed [6]. But iv dextrose needs NICU admission-costly, invasive, separates mother from baby increased maternal anxiety and interfere breast feeding establishment. Severe or prolonged hypoglycemia persistent high or ongoing ≥ 3 days iv glucose needs point underlying metabolic or endocrine pathology. Escalated insulin-hyper insulins-suppresses alternate fuel generation thus sustain glucose > 3.5 mmol/l [6]. Extra treatment glucagon, diazoxide or glucocorticoids might needed [6]. Oral dextrose gel 200 mg/kg of 40% dextrose along with feeding advocated-1^st line treatment in asymptomatic NH [10]. A RCT of 237 late preterm and term babies with NH (< 47mg/dl [2.6 mmol/l)) documented in contrast to feeding only, 40% oral dextrose gel 200 mg/kg feeding lesser treatment failures (dec NICU admission advocated in various national guidelines. ProphylaxisSome proof even transient and undetected NH side effects, study of 1395 babies in centre with glucose screening demonstrated single episode TNH (< 35 mg/dl was correlated with lower 4^th grade literacy and numeral proficiency at 10yrs [11]. Children with hypoglycemia and their later development (CHYLD) study showed clinically not detected low interstitial glucose amounts was correlated with escalated executive function impairment at 4.5yrs age [12]. Currently advocated-early feeding, ensure babies warm and dry with early skin contact. Further oral dextrose gel being tested in at risk babies with early BF outcomes-MRI studies NH can brain damage. Commonest ABI located in parietal and occipital areas implicated in visual processing still inconsistent if later visual problems [13]. Adequately powered RCT s required to see for both prophylactic and treatment interventions at several glucose thresholds with neuro developmental dysfunction evaluated at least till school age. Significance of this lies in encountering of a newborn term infant who developed TN H without any at risk factors presenting as listless, cold in hot environment with mother receiving epidural anaesthesia with single reading of 35 mg-recovered with immediate 10% dextrose and feeding although later sugars all above 58 mg.

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