Therapeutic hypothermia in neonatal encephalopathy-Challanges.pptx

Therapeutic hypothermia in neonatal encephalopathy-Challanges

1. Therapeutic hypothermia in neonatal encephalopathy: current challenges and future prospects

2. Intro Hypoxic–ischemic encephalopathy (HIE) is a major cause of mortality and long-term neurodevelopmental impairment globally. Currently, therapeutic hypothermia (TH) represents the only evidence-based neuroprotective treatment for moderate-to-severe neonatal HIE, having resulted in consistent reductions in rates of mortality and disability. However, despite its success in advanced healthcare settings, challenges persist regarding its universal implementation, particularly in low- and middle-income countries (LMICs). This review examines the evolution of TH and outlines the challenges and controversies regarding this therapeutic approach.

3. Applying TH in resource-constrained settings It also explores the complexities of applying TH in resource-constrained settings, the debates about its use in mild HIE and preterm infants, and the limitations of current diagnostic and prognostic tools such as conventional MRI and amplitude-integrated EEG. it discusses the emerging approaches aiming to enhance the effectiveness and precision of TH. These include adjuvant therapies, improved neuroimaging modalities, and the identification of new biomarkers to better predict outcomes and individualize care.

4. HIE and TH: an overview Typically, HIE results from a significant reduction in oxygen (hypoxia) and/or blood flow (ischemia) to the fetal or neonatal brain, often occurring during labor, delivery, or the immediate postnatal period. This insult initiates a complex biphasic pattern of brain injury, which unfolds over time and contributes to neuronal mortality and neurodevelopmental impairment

5. Mechanism of TH Therapeutic hypothermia has emerged as an evidence-based neuroprotective intervention for infants with moderate-to-severe HIE, reducing the risk of combined death or disability by 20– 30% . The neuroprotective effects of TH are primarily exerted during the latent phase, aiming to interrupt or attenuate the secondary energy failure. By lowering the core body temperature to 33–34 ◦ C for 72 h, TH slows cerebral metabolism, reduces oxygen and energy demand, and mitigates excitotoxicity.