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Neonatal Hyperbilirubinemia and Hypoglycemia

Hyperbilirubinemia in Neonates

  • Opening context

    • Jaundice is a visible sign of hyperbilirubinemia and is not exclusive to newborns; adults can have jaundice from liver disease, but in newborns it often reflects liver immaturity.
    • The liver in newborns is large relative to abdomen (about 40\% of the abdomen) but does not function at full capacity yet, which affects clotting and waste filtration, including breakdown of red blood cells.
    • Red blood cells (RBCs) break down into hemoglobin and then bilirubin. In simple terms: damaged/red blood cells turn into bilirubin.
  • Why bilirubin rises in newborns (risk factors and mechanisms)

    • Risk factors often involve increased RBC damage or turnover:
    • Polycythemia (high circulating RBC volume)
    • ABO and Rh incompatibilities
    • Birth trauma leading to bruising (e.g., cephalohematoma)
      • Cephalohematoma: bleeding under the scalp that stays on one side and does not cross sutures; associated edema and local RBC breakdown
    • Bruising/hematomas from birth
    • Preterm birth
    • Breastfeeding (breastfeeding jaundice)
    • Asian and Native American ancestry
    • Prior sibling who received phototherapy
    • In short: more damaged RBCs → more bilirubin production
    • Key reference: Box 22.2, page 520 in the textbook provides detailed risk factors
  • Jaundice types and their differences

    • Pathological jaundice
    • More extreme and higher bilirubin levels
    • Increases by more than 5\ \text{mg/dL per day} (i.e., >5\ \text{mg/dL/day})
    • Presents much earlier (often within the first 24 hours after delivery)
    • Tends to persist longer (usually longer than 7–14 days)
    • Often underlying baby-specific pathology driving high bilirubin
    • Physiological jaundice
    • Occurs in a majority of newborns; estimates from textbooks: \approx 60\% or more
    • Generally not alarming; monitored to ensure levels do not become too high
    • Typically resolves as liver matures (levels fall after an initial rise)
    • Practical takeaway: distinguish pathological vs physiological by onset timing, rate of rise, peak level, and duration
  • Monitoring and assessment: screening and thresholds

    • Transcutaneous bilirubin (TCB) testing (transcutaneous bili testing, often called TCB or TCV in practice)
    • External monitor (placed on forehead or sternum) to estimate bilirubin level
    • If TCB reading is above 12{$-14$} to 14-15\ \text{mg/dL}, a serum bilirubin (heel-stick) is drawn for confirmation
    • TCB is not as accurate as a serum bilirubin; used as initial screening
    • Timing: commonly performed around 18-24\ \text{hours} after birth
    • Serum bilirubin (yellow blood test) for confirmation and more accurate measurement when TCB is elevated
    • Normalized management concept: use the risk zone approach based on hours of life
    • Low risk, low intermediate risk, high intermediate risk, high risk zones
    • Chart (PowerPoint slide 28) shows how bilirubin levels relate to age in hours
    • Around 72\ \text{hours} (day 3–5), bilirubin levels peak for many babies
    • Physiological jaundice: bilirubin typically peaks and then declines by days 7-14
    • Pathological jaundice: higher risk zones (high intermediate/high) persist and may require intervention
    • Example interpretation (from clinical notes): a bilirubin level above 7\ \text{mg/dL} within the first 24 hours would place the baby in a high intermediate/high risk zone
  • Interventions and treatment approaches

    • Early feeding to reduce bilirubin risk
    • Frequent feedings are recommended for every baby, even before confirming a diagnosis
    • Phototherapy (BiliLights)
    • Indicated when bilirubin levels are high and/or rising; phototherapy helps reduce bilirubin levels
    • Practical setup: baby placed under BiliLights with eye protection (glasses) and a diaper on to protect genitals
    • Maintain body temperature and monitor skin for breakdown
    • Rotate position every couple of hours to maximize exposure
    • Ensure regular feeding to promote bilirubin excretion via urine and stool
    • Do not apply lotion or other topical agents to simulate tanning; no extra skincare tricks beyond standard phototherapy care
    • Location: phototherapy can be done on postpartum floors in many facilities; NICU involvement depends on overall clinical course and stability
    • Serum bilirubin monitoring and thresholds for phototherapy
    • If TCB reads high (e.g., above 12-15\ \text{mg/dL}), obtain a serum bilirubin to confirm level
    • Exchange transfusion (rare, but a fallback option)
    • Considered if phototherapy is not effective or if bilirubin remains dangerously high
    • Mechanism: remove a small portion of the baby’s blood and replace with donor blood to rapidly reduce bilirubin
    • Described proportionally: remove 5-10\ \text{cc} and replace with the same amount; repeat as needed
    • Not commonly seen; attention-worthy when encountered
  • Complications and safety considerations

    • Kernicterus (acute or chronic bilirubin encephalopathy)
    • Serious risk when bilirubin levels are very high or persist
    • Bilirubin can deposit in the brain (cerebellum and brainstem) causing irreversible neurologic deficits
    • Threshold mentioned: risk increases with bilirubin levels \ge 25\ \text{mg/dL} and persistent high levels
    • Early recognition and treatment are critical to prevent long-term neurologic damage
    • Signs with high bilirubin that prompt urgent assessment
    • High-pitched cry is a warning sign suggesting possible encephalopathy or acute bilirubin-related neurotoxicity
  • Practical notes and occurrences in care settings

    • Phototherapy details
    • Baby protection: eye protection (glasses) and diaper to minimize genital exposure
    • Skin exposure is important for bilirubin breakdown; avoid occlusive skincare products
    • Frequent monitoring and temperature checks
    • Testing logistics
    • TCB/TCV for screening, then serum bilirubin for confirmation if levels are elevated
    • Unit placement considerations
    • Bilirubin lights are commonly used on postpartum floors; NICU referral depends on stability and other conditions
  • Brief recap of the cited references from the session

    • Textbook reference: Box 22.2, page 520 (risk factors for hyperbilirubinemia)
    • Safety and diagnostic notes: Box entries on pathological vs physiological jaundice (page 520)
    • Slide reference: PowerPoint slide 28 (normal newborn care) shows the risk zones and hours-based interpretation
  • Transition to hypoglycemia (brief segue from the session)

    • Hypoglycemia is presented as a common neonatal complication alongside hypothermia
    • High-risk groups for neonatal hypoglycemia (as discussed in the session):
    • Large babies (macrosomic)
    • Infants of diabetic mothers
    • Premature babies
    • Small for gestational age (SGA)
    • Mechanisms of neonatal hypoglycemia
    • Hyperinsulinemia: babies of diabetic mothers or macrosomic babies produce excess insulin; after birth, the abrupt cut of maternal glucose via the umbilical cord leads to glucose depletion
    • Limited glycogen stores: especially in preterm or SGA babies; glycogen stores are typically exhausted quickly (the lecturer noted depletion within the first 90 minutes to 3 hours after birth)
    • Management emphasis (as mentioned in the session)
    • Early, frequent feeding to prevent or treat hypoglycemia
    • Note: The hypoglycemia section cuts off mid-discussion in the transcript, but the key risk factors and mechanisms are covered above
  • Quick reference points for exam-style review

    • Normal neonatal liver function is immature; bilirubin handling is limited early on, increasing bilirubin risk
    • Major risk factors: birth trauma (cephalohematoma), ABO/Rh incompatibility, polycythemia, prematurity, breastfeeding, certain ethnicities, and prior sibling phototherapy
    • Pathological jaundice: onset within 24 hours, rapid rise (> 5\ \text{mg/dL/day}), persists beyond 7–14 days
    • Physiological jaundice: common in >50–60% of newborns; peaks around 72\ \text{hours}, resolves by days 7–14
    • Assessment pathway: screen with TCB/TCV; confirm with serum bilirubin if elevated (threshold around 12-15\ \text{mg/dL})
    • Treatment: early feeding for all; phototherapy for high levels; exchange transfusion as a rare escalation
    • Critical threshold: kernicterus risk rises with bilirubin \ge 25\ \text{mg/dL} or prolonged high levels
    • Signs of concern: high-pitched cry, persistent jaundice, scleral icterus, changing neurobehavioral status
  • Page references for quick lookup

    • Box 22.2, page 520 (risk factors for hyperbilirubinemia)
    • Physiological vs pathological jaundice discussion, page 520$$
    • Normal newborn care chart, PowerPoint slide 28
  • Note for study planning

    • Review the distinctions between physiological and pathological jaundice, and the clinical thresholds used to trigger phototherapy or further testing
    • Familiarize yourself with the workflow: screen with TCB/TCV, confirm with serum bilirubin, initiate early feeding, apply phototherapy with eye/skin precautions, monitor for signs of kernicterus, and know when an exchange transfusion is considered