Neonatal hypoglycaemia

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  • Erythroblastosis: hyperplastic islets of Langerhans Beckwith-Wiedemann: macrosomia, mild microcephaly, omphalocele, macroglossia, hypoglycaemia, visceromegaly Nesiodioblastosis:  cell hyperplasia Maternal drugs: Tocolytic therapy with  sympathomimetic agents (terbutaline, albuterol, salbutamol), chlorpropamide (sulphonylurea - increases insulin release)
  • Polycythaemia:  glucose utilisation by  red cell mass Exchange transfusion: With blood that has a low glucose level with a glucose infusion or reactive hypoglycaemia following exchange with hyperglycaemic blood Congenital heart disease Maternal propranolol: 1. Prevention of sympathetic stimulation of glycogenolysis 2. Prevention of recovery from insulin-induced decreases in free FAs & glycerol 3. Inhibition of epinephrine-induced increases in free FAs & lactate after excercise
  • Screening using glucose reagent strips - unproven reliability bcos: 1. Reagent strips measure whole blood glucose, which is 15% lower than plasma levels 2. False positive / false negative Glucose level can fall 18mg/dl per hour in blood sample that awaits analysis
  • Somatostatin: long acting, octreotide acetate
  • Neonatal hypoglycaemia

    1. 1. Neonatal Hypoglycaemia Dr Varsha Atul ShahDept of Neonatal and Developmental Medicine Singapore General Hospital
    2. 2. Extremes of Birth WeightNeonatalHypoglycaemia Prematurity
    3. 3. Definition• Controversial• Operational threshold – Pragmatic approach – i.e. blood glucose level at which clinical intervention should be considered – Indication for action but not diagnostic of disease – Symptomatic: < 45mg/dl (2.5mmol/L) – Asymptomatic & at-risk: < 36mg/dl (2.0mmol/L)
    4. 4. • Significant neonatal hypoglycaemia (Whipple’s triad) – Clinical manifestations – Coincident low plasma glucose level (laboratory) – Clinical signs resolve within mins - hrs of establishing normoglycaemia• Therapeutic objective – Raise plasma glucose level > 45mg/dl (2.5mmol/L)
    5. 5. • Term breastfed infants – Can utilise ketones as source of energy in absence of glucose during transient starvation – May tolerate low glucose levels better
    6. 6. Clinical Features• Non specific – Apathy, lethargy, irritability – Hypotonia, limpness – Sweating, tremors, jitteriness, abnormal cry (weak / high pitched) – Hypothermia – Poor feeding, vomiting – Apnoea, irregular respiration, respiratory distress, cyanosis – Tachycardia, CCF – Seizures, coma• Asymptomatic
    7. 7. Aetiology∀ ↑ utilisation of glucose: hyperinsulinism (Hyperinsulinism: inhibit glycogenolysis & gluconeogenesis) – Infant of diabetic mother (IDM) – Erythroblastosis – Beckwith-Wiedemann syndrome – Islet-cell hyperplasia / hyperfunction – Insulin-producing tumours (nesidioblastosis, islet-cell adenoma) – Maternal drugs (salbutamol, chlorpropamide) – Abrupt cessation of high-glucose infusions
    8. 8. Infant of diabetic mum“Cherubic” facies
    9. 9. Beckwith-WiedemannSyndromeMacrosomia, macroglossia,omphalocele, hypoglycaemia,microcephaly
    10. 10. ∀ ↓ production/stores – Prematurity – Intrauterine growth retardation – Inadequate caloric intake Premature IUGR
    11. 11. ∀ ↑ utilisation and/or ↓ production or others – Stress • Sepsis (↑ utilisation) • Shock • Asphyxia (↓ stores) • Hypothermia (↑ utilisation) – Polycythaemia (↑ utilisation by ↑ red cell mass) – Exchange transfusion – Inborn errors of metabolism – Defect in carbohydrate metabolism • Glycogen storage disease, fructose intolerance, galactosemia – Defect in amino acid metabolism • Maple syrup urine disease, propionic acidemia, etc – Endocrine causes – Adrenal insufficiency, hypothalamic deficiency, congenital hypopituitarism, glucagon deficiency, epinephrine deficiency
    12. 12. Management• Prevention – Antenatal & intrapartum care • e.g. control of maternal diabetes, causes of prematurity & IUGR – Avoid environmental stress e.g. cold – Early feeding / IV dextrose infusion
    13. 13. • Anticipation – Screening 1. At-risk babies a. Maternal e.g. drugs, intrapartum glucose, diabetes, etc b. Neonatal e.g. asphyxia / perinatal stress, premature, SGA / LGA, low birth weight, sepsis, shock, polycythaemia, etc 2. Those with symptoms Non specific; high index of suspicion
    14. 14. • Diagnosis – Screening using glucose reagent strips • Within 2 - 3 hrs after birth & before feeding (2 - 4 hrly) for 24 - 48 hrs & whenever symptomatic – Confirmatory laboratory diagnosis important • Do not delay treatment while waiting for result • Analysed promptly to avoid falsely low value due to glycolysis
    15. 15. • Treatment – Aim to maintain plasma glucose > 45mg/dl (2.5mmol/L) – IV dextrose • Mini bolus Dex 10% (2ml/kg) followed by infusion • Central line required for high dextrose concentrations (> Dex 10%) • Continued close plasma glucose monitoring to titrate infusion • Avoid abruptly decreasing dextrose infusion (rebound hypoglycaemia)
    16. 16. – Adjunct therapy • Considered if persistent hypoglycaemia despite glucose infusion > 10-12mg/kg/min • Glucagon: stimulates glycogenolysis (adequate glycogen stores) (AGA/LGA) • Hydrocortisone: ↓ peripheral glucose utilisation, ↑ gluconeogenesis, ↑ glucagon effects (prem/SGA) • Rarely: – Diazoxide: inhibits insulin secretion – Somatostatin: inhibits insulin & growth hormone release – Subtotal pancreatectomy: decreases insulin release (insulin-secreting tumours)
    17. 17. • Most hypoglycaemia resolve in 2 - 3 dys• Persistent / recurrent hypoglycaemia for > 1 week may require evaluation for other causes – e.g. insulin, cortisol, other endocrine & insulin IEM studies during period of hypoglycaemia• During a period of hypoglycaemia, a normal infant’s blood insulin level should be low or absent. If it is very high suggests hyperinsulinism. It inhibits braeking down of glyconen
    18. 18. Significance of Hypoglycaemia• Neuronal cell injury, cerebral damage, long term neurologic sequelae• No single value below which or duration beyond which brain injury definitely occurs• ? Vulnerability of brain of infants of different gestational ages• Prevention, prompt treatment important
    19. 19. Symmetric patchyhyperintensities in occipitalwhite matter in brain of infantwith transient neonatalhypoglycaemia Kinnala Peds 1999
    20. 20. T2 weighted axial MRI at 10 months of ageBoy with isolated hypoglycaemia: shows parenchymal loss posteriorly withcomputed tomography at 6 days of high signal in the white matter of theage shows cortical and white matter parietal and occipital lobes (arrows). Notelow density that is most severe in thin and atrophic gyri (arrowhead)the parietal and occipital lobes Traill, Arch Dis Child 1998
    21. 21. Boy with a variant of glycogen T2 weighted axial magnetic resonance imagestorage disease type 2b. Computed at 7 years of age shows marked atrophy intomogram at 6 days of age shows low the parietal and occipital cortex anddensity in the cortex and white underlying cerebral white mattermatter of the parietal and occipitallobes Traill, Arch Dis Child 1998
    22. 22. Outcome• Varied• Some have no long term sequelae• Symptomatic / severe / persistent hypoglycaemia – Abnormal neurointellectual development
    23. 23. – Cerebral palsy– Epilepsy– Cognitive impairment– Visual problems– Developmental & behavioural disorders
    24. 24. Long Term Management• Neurodevelopmental follow up to identify sequelae of neuroglycopenia• Identify growth deficits

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