ArticleJournal of perinatology : official journal of the California Perinatal Association2026
Defining the 'Hypothermia Resistant' phenotype in neonatal HIE: persistent multi-organ dysfunction on day 3 is the hallmark of MRI injury.
Article in Journal of perinatology : official journal of the California Perinatal Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTherapeutic hypothermia (TH) reduces mortality in neonatal hypoxic-ischemic encephalopathy (HIE), yet nearly half of treated infants suffer adverse outcomes. This study aimed to define the "Hypothermia Resistance" phenotype by characterizing the 4-day trajectories of multi-organ dysfunction and identifying the physiological signals associated with severe MRI injury. STUDY
designThis retrospective cohort study included 24 term neonates with moderate-to-severe HIE treated with whole-body hypothermia. Patients were stratified into "Responder" (n = 18) and "Resistant" (n = 6) phenotypes based on systemic recovery patterns. Serial biomarkers (Lactate, Creatinine, AST, Platelets) were analyzed daily from Day 1 to Day 4. The primary outcome was brain injury severity on MRI assessed by the Weeke score.
resultsAdmission characteristics and Day 1 biomarkers were comparable between groups. However, trajectories diverged significantly by Day 3 (72 h). The Resistant phenotype was characterized by a failure to clear systemic dysfunction, manifesting as persistent renal impairment (Median Creatinine: 1.39 vs 0.65 mg/dL; p < 0.01) and worsening thrombocytopenia (Median Platelets: 114 vs 190 × 10³/µL; p < 0.05) at 72 h. This "Day 3 Cliff" profile (Creatinine >1.0 mg/dL combined with Platelets <120 × 10³/µL) was strongly associated with severe MRI injury (diffusion restriction in basal ganglia/thalamus).
conclusionPhysiological recovery during cooling is a dynamic process. Persistent multi-organ dysfunction on Day 3 constitutes a "Hypothermia Resistance" profile that serves as a robust surrogate marker for ineffective neuroprotection, distinct from early severity markers.
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