neonatal hypoglycaemia
TRANSCRIPT
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Neonatal Neonatal HypoglycaemiaHypoglycaemia
Dr Varsha Atul Shah
Dept of Neonatal and Developmental Medicine
Singapore General Hospital
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Extremes of Extremes of Birth WeightBirth Weight
Neonatal Neonatal HypoglycaemiHypoglycaemiaa
PrematurityPrematurity
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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)
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• 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)
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• Term breastfed infants– Can utilise ketones as source of energy in
absence of glucose during transient starvation
– May tolerate low glucose levels better
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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
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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
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Infant of diabetic mum
“Cherubic” facies
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Beckwith-Wiedemann Syndrome
Macrosomia, macroglossia, omphalocele, hypoglycaemia, microcephaly
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production/stores– Prematurity– Intrauterine growth retardation– Inadequate caloric intake
IUGR
Premature
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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
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• 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
Management
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• Anticipation– Screening
1. At-risk babiesa. Maternal
e.g. drugs, intrapartum glucose, diabetes, etcb. 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
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• 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
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• 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)
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– 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)
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• Most hypoglycaemia resolve in 2 - 3 dys
• Persistent / recurrent hypoglycaemia for > 1 week may require evaluation for other causes– e.g. insulininsulin, cortisol, other endocrine &
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
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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
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Symmetric patchy hyperintensities in occipital white matter in brain of infant with transient neonatal hypoglycaemia
Kinnala Peds 1999
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Boy with isolated hypoglycaemia: computed tomography at 6 days of age shows cortical and white matter low density that is most severe in the parietal and occipital lobes
T2 weighted axial MRI at 10 months of age shows parenchymal loss posteriorly with high signal in the white matter of the parietal and occipital lobes (arrows). Note thin and atrophic gyri (arrowhead)
Traill, Arch Dis Child 1998
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Boy with a variant of glycogen storage disease type 2b. Computed tomogram at 6 days of age shows low density in the cortex and white matter of the parietal and occipital lobes
T2 weighted axial magnetic resonance image at 7 years of age shows marked atrophy in the parietal and occipital cortex and underlying cerebral white matter
Traill, Arch Dis Child 1998
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Outcome
• Varied
• Some have no long term sequelae
• Symptomatic / severe / persistent hypoglycaemia– Abnormal neurointellectual development
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– Cerebral palsy– Epilepsy– Cognitive impairment– Visual problems– Developmental & behavioural disorders
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Long Term Management
• Neurodevelopmental follow up to identify sequelae of neuroglycopenia
• Identify growth deficits
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