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Practice Points:  Neonatal encephalopathy (NE) is a clinical diagnosis which may arise from numerous etiologies HIE may be distinguished from NE due to other causes using the history, physical and neurological exam, and investigations PubMed Link To view the full text and an associated presentation, become a NBS member here

Practice Points:  Therapeutic Hypothermia is a safe and effective treatment which reduces the impact of neural injury following hypoxia ischaemia and moderate/severe neonatal encephalopathy. Despite TH, a high proportion of survivors still develop moderate/ severe disability necessitating close follow up into childhood designed to identify neuromotor, cognitive and behavioural prob- lems. Early referral to child

Practice Points:  Neuroimaging in the term neonates with neonatal encephalopathy (NE) is useful to identify patterns consistent with hypoxic-ischemic brain injury, to inform management decisions, to prognosticate long-term outcome, and to rule out other etiologies than hypoxic- ischemic brain injury. Magnetic resonance imaging is the preferred imaging technique for examining the brain of term neonates

Practice Points:  EEG/aEEG While aEEG is helpful to monitor trends at the bedside and can diagnose most seizures, cEEG remains the gold standard for seizure detection. Because of the wide range of start time and frequency of seizures, it is recommended to use either cEEG/aEEG throughout therapeutic hypo- thermia and rewarming, with a minimum of

Practice Points:  Communication amidst therapeutic hypothermia is challenging; parents desire timely, transparent, and consistent communication with clinicians. Parents value opportunities to participate in their infant’s clinical care. Programs should work to integrate parents into clinical care in the acute period and empower them to lead clinical care and rehabilitation as they prepare for life at

Practice Points:  The evolution of injury following hypoxic-ischemic injury involves multiple mechanisms and progresses over a prolonged period of time. Cell death often presents as a continuum between early necrosis and later apoptosis, involving a balance between early biophysical damage and failure of oxidative metabolisms and activation of pro- grammed cell death pathways. Very delayed

Practice Points:  Clinicians looking after neonates with NE treated with TH must be aware of SFNN and must be assessed the neonates routinely for SFNN Routine clinical and biochemical monitoring for hypercalcemia in those with SFNN or at-risk is critical Hypercalcemia is typically detected at a month of age; half the neonates are asymptomatic Prompt

Practice Points:  Non-pharmacologic approaches form the foundation for providing comfort for neonates with NE receiving TH Benzodiazepines should be avoided for sedation Morphine 50 μg/kg followed by a continuous infusion of 5 μg/kg/hour currently represents the approach to pharmacologic sedation with the strongest basis in evidence Low-dose dexmedetomidine infusion may be considered as an alternative

Practice Points:  Haematological abnormalities are common in neonates with neonatal encephalopathy (NE), including leukocytosis, thrombocytopenia and coagulopathy. nRBCs and EPO may indicate the degree of exposure to hypoxia in neonates with NE. Leukocytes are elevated in NE and associated with systemic inflammation. Consensus on thresholds for intervention are lacking, as there is a relative paucity

Practice Points:  Thresholds for hypoglycemia and hyperglycemia remain poorly defined and may vary depending on comorbid conditions and impaired metabolic adaptations. Glycemic levels should be maintained within the broadly accepted physiologic ranges during the early postnatal period in neonates with NE. Hypoglycemia and hyperglycemia in neonates with NE are associated with worse neurodevelopmental outcomes. Optimal