Issue: 2026, Vol. 31, No. 2

I. I. Polikarpova, E. P. Sitnikova, I. A. Leontiev

BIDIRECTIONAL RELATIONSHIP BETWEEN CEREBRAL ISCHEMIA AND NEONATAL JAUNDICE: DEVELOPMENT OF A VICIOUS CYCLE IN NEONATES

Keywords

neonatal jaundice, cerebral ischemia, hypoxic-ischemic central nervous system injury, bilirubin encephalopathy, nonlinear dynamic systems, vicious cycle

Abstarct

Objective – to examine the interrelationship between cerebral ischemia and neonatal jaundice through the lens of dynamic systems theory, substantiating the need for early preventive complex intervention. Materials and Methods. This single-center cohort study included 83 newborns with conjugation hyperbilirubinemia. Clinical data and patient history were analyzed, followed by bilirubin assessment and cerebral Doppler ultrasound. Based on the presence of hypoxic-ischemic central nervous system injury, patients were stratified into a main group (n = 52) and a comparison group (n = 31). Statistical analysis was conducted using Student’s t-test and χ² (chi-square) test (p < 0.05). One-way analysis of variance (ANOVA) was applied for subgroup comparisons. Results and Discussion. The prevalence of cerebral ischemia among newborns with jaundice was 63 %, significantly exceeding population-based rates (χ² = 12.47; p < 0.01). The main group demonstrated a higher peak bilirubin level (by 18–22 %) and prolonged duration of jaundice (by 3.2 days; p < 0.05). These infants also required repeat phototherapy substantially more often (38 vs 12 %; p < 0.01) and exhibited neurological disorders at a markedly higher frequency. Doppler ultrasonography in the main group revealed an elevated resistive index in the anterior cerebral artery, indicating increased vascular resistance and microcirculatory impairment. Cerebral ischemia and hyperbilirubinemia form two interconnected positive feedback loops. Ischemia increases blood-brain barrier permeability, disrupts gastrointestinal function, and impairs microcirculation, thereby prolonging jaundice. Conversely, unconjugated bilirubin exacerbates ischemic injury through mitochondrial dysfunction, excitotoxicity, and neuroinflammation. A critical threshold exists, beyond which irreversible bilirubin encephalopathy develops. Conclusion. Cerebral ischemia and neonatal jaundice constitute a unified nonlinear dynamic system with mutual aggravation. A shift toward a preventive strategy is warranted: early initiation of phototherapy (at bilirubin levels 50–70 μmol/L below standard thresholds), intensive monitoring, and comprehensive management. Infants with combined pathology require neurological follow-up for at least two years.

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• Quid est Veritas-11-19