0.64 CME

नवजात हाइपोग्लाइसीमिया

वक्ता: डॉ सुब्रत डे

Senior Pediatric Endocrinologist at Apollo Gleneagles Hospital, Kolkata

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विवरण

Neonatal hypoglycemia refers to low blood sugar levels in newborns, a condition that can occur within the first few days of life.It is most commonly seen in infants born to mothers with diabetes, preterm infants, or those with intrauterine growth restriction. The developing brain is highly sensitive to glucose levels, making neonatal hypoglycemia a concern due to its potential impact on neurological development. Symptoms of neonatal hypoglycemia may include jitteriness, poor feeding, lethargy, and, in severe cases, seizures. Early identification and monitoring of at-risk infants are crucial to prevent long-term complications associated with low blood sugar levels.

Interventions often involve adjusting feeding practices, such as more frequent breastfeeding or formula supplementation, to maintain optimal glucose levels.Point-of-care glucose monitoring and laboratory tests are used to assess and manage neonatal hypoglycemia. Timely and appropriate treatment is essential to prevent complications, as persistent low blood sugar levels can lead to neurological deficits.Neonates born to mothers with gestational diabetes may be closely monitored, as they are at an increased risk of hypoglycemia. The management of neonatal hypoglycemia requires a multidisciplinary approach involving neonatologists, pediatricians, and nursing staff to ensure optimal care and neurodevelopmental outcomes.

सारांश

  • Neonatal hypoglycemia, characterized by low blood sugar in newborns, lacks a universally accepted definition. While a blood glucose level below 40 mg/dL often warrants intervention, clinical significance hinges on individual risk factors, signs, and metabolic adaptation, with no specific threshold definitively causing brain damage. Infants at higher risk include preterm babies, those large or small for gestational age, those born to diabetic mothers, and those experiencing perinatal stress.
  • The transition from fetal to neonatal life involves a shift from maternal glucose dependency to independent hormonal regulation. The fetus receives glucose through placental diffusion, but after birth, this supply is interrupted, leading to insulin suppression and the activation of counter-regulatory hormones like glucagon, cortisol, and adrenaline. This triggers glycogenolysis, gluconeogenesis, and ketogenesis, processes crucial for maintaining glucose levels, though premature infants often lack sufficient glycogen stores.
  • Management of neonatal hypoglycemia involves careful monitoring and intervention based on operational thresholds. Protocols like the as protocol dictate interventions based on blood glucose levels and symptom presentation, including oral feeds or IV dextrose. American Academy of Pediatrics guidelines suggest initial feeding within the first hour, followed by glucose screening and intervention as needed. The pediatric endocrine society recommends treatment targets based on postnatal age, with higher thresholds for suspected congenital hypoglycemic disorders.
  • Persistent or refractory hypoglycemia, characterized by high glucose infusion rates beyond 48 hours, requires specialized investigation. A "critical sample" including insulin, cortisol, growth hormone, beta-hydroxybutyrate, free fatty acids, lactate, and ammonia is essential for diagnosis. Conditions like hyperinsulinism, hypopituitarism, and inborn errors of metabolism must be considered, guiding further management strategies that may include diazoxide, octreotide, genetic testing, or even surgical intervention.
  • Hyperinsulinism diagnosis relies on critical sample criteria such as elevated insulin levels and inappropriate glucagon response. Differentiating between types of inborn errors of metabolism requires careful assessment of metabolite profiles. Glucagon stimulation tests serve as the gold standard for hyperinsulinism diagnosis. Management pathways involve assessing for diazoxide responsiveness, considering genetic analysis for specific mutations, and potentially pursuing dopa-CT scans to differentiate between focal and diffuse disease, ultimately guiding treatment strategies like diet modification, medication, or partial pancreatectomy.

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