Neonatal hypoglycemia

 DEFINITION
 PATHOPHYSIOLOGY
 ETIOLOGY
 SCREENING
 MANAGEMENT
INTRODUCTION

 Glucose provides approximately 60% to 70% of fetal energy needs.

 All newborns depend on maternal source for glucose
 The severing of the umbilical cord at birth abruptly interrupts the source of glucose.
 During this normal transition, new born glucose levels fall to a low point in the first one to two hours of life
and then increase to > 45mg/dl,
.
DEFINITION

Various glucose levels are used to describe hypoglycemia, AAP and Paediatric endocrine society guidelines
are most widely used to provide margin of safety.
Based on Symptomatic – newborn <48 hours of life-if glucose is <50mg/dl of plasma glucose.
new born is age >48 hrs of life- hypoglycemia <60mg/dl.
Asymptomatic-At risk
<4hrs of life-glucose <25mg/dl
4 and 24hrs-glucose<35mg/dl
24-48hrs-glucose <50 mg/dl
>48hrs-Glucose<60mg/dl
AT RISK

 Birth weight <2 kg or >4 kg

 Large for gestational age (LGA)
 Small for gestational age (SGA)
 Intra uterine growth restriction (IUGR)
 Neonates of insulin dependent mother (1:1000 pregnant women)
 Mothers with gestational diabetes (-2% of pregnant women)
 Preterm or late preterm neonates.
 Suspected of sepsis or chorioamnionitis
 Significant hypoxia
 Perinatal distress
 Hypothermia
 Isolated hepatomegaly
 Microcephaly
 Multiple congenital anomalies
 Suspected in born error of metabolism
 Maternal history of terbutaline, betablockers, or oral hypoglycemic medications
PATHOPHYSIOLOGY

 Hormones which regulate glucose levels

 -Insulin
 -Glucagon
 When glucose levels fall
 •Glycogen is secreted to increase glucose levels through glycogenolysis
 •Glycogenolysis releases glucose back into the blood
ETIOLOGY

 Inappropriate changes in hormone secretion

 Inadequate substrate reserve-Hepatic glycogen
 Inadequate muscle stores
 Source of amino acids for gluconeogenesis
 Inadequate lipid stores
 Release of fatty acids
ETIOLOGY

 Hyperinsulinemic-Increased insulin-more glucose utilization

a)IDM
b)CONGENITAL- GENETIC-SUR1,Kir6.2
c) SECONDARY TO OTHER CONDITION LIKE –birth asphyxia,Beckwith wiedemann
syndrome,erythroblastosis,maternal tocolytic therapy-terbulatin,malposition of umbilical artery catheter,at level
T11-T12-stimulate insulin release,abrubt cessation of high glucose infusion,after exchange transfusion,insulin
producing tumors
 Decreased production/stores
Prematurity,IUGR/SGA,poor intake,delayed feeding
 Increased utilization-Perinatal stress,after exchange transfusion,
 Defect in CHO metabolism
 Endocrine deficiency
 Defects in aminoacid metabolism
 Polycythemia-due to increased red cells-inturn utilize more glucose
 Maternal/infant therapy-B blockers-labetalol,
 SIGNS AND SYMPTOMS

Fall into two categories

 -Neurogenic symptoms
•Affect activity along the sympathetic nervous system
•Are both adrenergic and cholinergic
 Adrenergic symptoms ,Anxiety, tremulousness,Tachycardia Palpitations
 -Cholinergic symptoms•Diaphoresis,Pallor,Hunger, nausea, and vomiting
 -Neuroglycopenic symptoms
•Due to brain dysfunction from a deficient glucose supply
 Hypotonia
 Lethargy, apathy
 Tachypnea, apnea
 Poor feeding
 Jitteriness, seizures
 Congestive heart failure
 Cyanosis
 Apnea
 Hypothermia, temperature instability
RECOMMENDATIONS

1) Symptomatic newborn with GRBS < 40mg/dl; patient with IV infusion

2) Symptomatic
a) In 1st 4 hours
i. If 1st hours <25mg/dl – give feeds , check again
if 35-45 then give feeds
if <25 then start infusion
ii. If suspending check in between 35-40 give feeds.
b) In next 24 hours
i. If glucose in <35mg /dl – initiate feed
ii. After feed <35 start infusion
iii. If.35-40mg/dl – start and continue feeds.
iv. target to maintain >45mg/dl
c) According to PES -48-72hr,
blood glucose – (glucometer) 50 mg/dl
glucose strips ± 10 -15 mg/dl varies ; and generally it is 15% lower than plasma levels
SCREENING

 Whom all to screen

 At high risk
 Inability to maintain preprandial plasma glucose levels
>50mg/dl in <48hours or glucose levels
>60 mg/dl in >48hrs of life
 Persistent hypoglycemia –requiring GIR of 8-10 mg/kg/min
 Evaluate-for Hyperinsulinemia-to send plasma glucose,cortisols,insulin,B hydroxybuterate and FFA,C
peptide
 If insulin is normal-then consider defect in metabolism of harmone
• T3,T4,TSH,Growth harmone
• ACTH
• Glucagon
• Plasma aminoacid
• Urine-reducing substtances, sugars,amino acids/Organic acids.
o Genitic analysis-SUR1,KiR6.2
Management

 Feeding
 GIR should be monitored(if requiring >12,then give via central line)
 Hydrocortisone-If GIR>12-15mgkg/min(10mg/kg/day Q8hry)-reduces peripheral glucose uptake,and inc
gluconeogenesis.
 Diazoxide 8-15mg/kg/day in Q12 hry/8th hrly(for hyper insulinemic state),
 Octreotide-5-20mg/kg/day-Sc/Iv Q8hry-Q6hrly.Long acting somatostatin analogue-inhibit insulin secretion.
 Glucagon-0.2mg/kg iv/sc/im
 Surgical correction.
 GIR calculation= DxR
6 x weight

 Ex -10 % dextrose,At 12 ml/hr and weight of baby is 3 kg= GIR=6.6mg/kg/min

LONG TERM OUTCOME

 Major long-term sequelae include

• -Neurologic damage
• •Mental retardation
• • Recurrent seizure activity, epilepsy
• • Cerebral palsy
• • Developmental delay
INBORN ERROR OF METABOLISM
ASSOCIATED WITH HYPOGLYCEMIA
TAKE AWAY MESSAGE

 To differentiate between symptomatic and asymptomatic hypoglycemia.

 At risk groups
 Early management
 GIR calculation,
 To know the outcomes.