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    Subjects/Pediatrics/Preterm and IUGR Baby Care
    Preterm and IUGR Baby Care
    medium
    smile Pediatrics

    Which of the following is the most common cause of neonatal hypoglycemia in preterm infants?

    A. Congenital adrenal hyperplasia
    B. Persistent hyperinsulinemic hypoglycemia of infancy
    C. Inadequate hepatic glycogen stores
    D. Fatty acid oxidation defects

    Explanation

    ## Neonatal Hypoglycemia in Preterm Infants ### Pathophysiology of Preterm Hypoglycemia **Key Point:** Preterm infants have immature hepatic enzyme systems and depleted glycogen stores, making them highly susceptible to hypoglycemia within the first 24–48 hours of life. Preterm infants (<34 weeks) have: - Reduced hepatic glycogen content (only 1–2% of liver weight vs. 5% in term infants) - Immature gluconeogenic enzymes (glucose-6-phosphatase, phosphoenolpyruvate carboxykinase) - Limited capacity for ketogenesis and fatty acid oxidation - High metabolic demands relative to energy stores ### Why Inadequate Hepatic Glycogen Stores Is Correct This is the **primary mechanism** in preterm infants. Glycogen deposition accelerates in the third trimester; preterm birth interrupts this process, leaving infants with critically low reserves. Hypoglycemia typically develops within 1–3 hours of birth if feeds are delayed. ### Differential Causes of Neonatal Hypoglycemia | Cause | Timing | Population | Key Feature | |-------|--------|------------|-------------| | **Inadequate glycogen stores** | 1–3 hrs, first 24–48 hrs | Preterm, SGA, cold stress | Most common in preterm | | **Persistent hyperinsulinemia** | Delayed (hours–days) | IDM, macrosomia, Beckwith–Wiedemann | High insulin suppresses hepatic output | | **CAH (21-hydroxylase deficiency)** | 3–7 days | Both sexes, salt-wasting variant | Cortisol deficiency impairs gluconeogenesis | | **Fatty acid oxidation defects** | Prolonged fasting | Rare genetic disorders | Presents later, with hypoketotic hypoglycemia | **High-Yield:** Preterm infants require early, frequent feeds (every 2–3 hours) and close glucose monitoring (heel-stick or continuous monitoring) in the first 48 hours to prevent symptomatic hypoglycemia. **Clinical Pearl:** Cold stress, sepsis, and respiratory distress syndrome increase glucose consumption and worsen hypoglycemia in preterm infants; maintaining normothermia and treating underlying illness are critical adjuncts to feeding. [cite:Nelson Textbook of Pediatrics 21e Ch 94]

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