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Published on: March 3, 2021
[Changes of brain edema after initiation of mild hypothermia therapy in children]
Keitaro Yamada1, Toshiyuki Mano, Yu Inada
1Department of Pediatric Neurology, Osaka Medical Center and Research Institute for Maternal and Child Health, Izumi, Osaka. keitaro_ymd1976@yahoo.co.jp
Insights
Mild hypothermia therapy shows potential for managing brain edema in children. Serial NSE measurements may help tailor treatment for conditions like hypoxic ischemic encephalopathy and acute encephalitis.
Area of Science:
- Pediatric Neurology
- Neurocritical Care
- Therapeutic Hypothermia
Context:
- Brain edema is a critical complication in pediatric neurological conditions.
- Hypoxic ischemic encephalopathy (HIE) and acute encephalitis/encephalopathy pose significant risks.
- Mild hypothermia therapy is explored as a neuroprotective strategy.
Purpose:
- To evaluate the efficacy of mild hypothermia (34°C) in mitigating brain edema in children.
- To identify potential biomarkers for monitoring treatment response and adjusting therapy.
- To compare outcomes in patients with HIE versus other encephalopathies.
Summary:
- Six children treated with mild hypothermia for brain edema were retrospectively analyzed.
- Two HIE patients showed no edema progression; two non-HIE patients experienced worsening edema.
- Delayed peak serum neuron-specific enolase (NSE) levels correlated with progressive edema.
Impact:
- Serial NSE measurement may serve as a valuable tool for personalizing hypothermia therapy.
- Findings suggest a need for further research into optimal hypothermia protocols, particularly for encephalitis.
- This study contributes to understanding therapeutic hypothermia's role in pediatric brain injury.
Abstract:
To determine the effects of mild hypothermia therapy (34 degrees C) for brain edema caused by hypoxic ischemic encephalopathy (HIE) or acute encephalitis/encephalopathy, we reviewed the charts and serial brain CT images in six children (males 3, average age 1.6 years) treated with mild hypothermia therapy between November 2006 and April 2009. Both of the two children with HIE after cardiopulmonary arrest did not show any deterioration of brain edema after the initiation of hypothermia therapy. However, two of four non-HIE patients (acute encephalitis/encephalopathy 3 cases and metabolic encephalopathy plus HIE 1 case) showed progressive brain edema during the cooling phase and re-warming phase, respectively. There were no differences between patients with and those without progressive brain edema with regard to the interval until initiation of mild hypothermia therapy, duration of cooling phase, duration of re-warming phase, or peak serum NSE (neuron-specific enolase) levels. However, two children with progressive brain edema showed a delayed NSE peak time (15 and 13 days after onset, respectively), compared with those without progressive brain edema (2-6 days after onset). Our study suggests that serial measurement of serum NSE might be useful marker for adjusting the methods of hypothermia therapy according to neuropathology. Further study is necessary to establish optimal hypothermia therapy especially in children with acute encephalitis/ encephalopathy.
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