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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Detailed clinical course of fatal acute encephalopathy in children
Kazumi Tomioka1, Masahiro Nishiyama1, Hiroaki Nagase1
1Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.
Insights
Fatal pediatric acute encephalopathy (AE) progresses rapidly, with systemic inflammatory response syndrome, shock, and disseminated intravascular coagulation developing within 14 hours. This study details the critical timeline of events in fatal AE cases.
Area of Science:
- Pediatric Neurology
- Critical Care Medicine
- Neuropathology
Background:
- Acute encephalopathy (AE) in children carries a significant mortality risk, yet its detailed clinical progression remains poorly understood.
- Understanding the temporal dynamics of fatal AE is crucial for timely intervention and improved patient outcomes.
Purpose of the Study:
- To meticulously document the clinical course, in minutes, of children who experienced fatal acute encephalopathy.
- To establish a precise timeline of neurological symptoms, systemic complications, and diagnostic milestones in fatal AE.
Main Methods:
- Retrospective analysis of medical records from five pediatric patients diagnosed with brain death due to AE.
- Inclusion criteria: previously healthy children (6 months to 14 years) with no prior neurological disorders, diagnosed between 2002 and 2018.
- Data collection focused on the timing of neurological symptoms, diagnostic findings, systemic inflammatory response syndrome (SIRS), disseminated intravascular coagulation (DIC), shock, and initiation of treatments.
Main Results:
- Initial symptoms included convulsions or impaired consciousness, with the earliest brain imaging abnormality appearing 7.5 hours post-symptom onset.
- All patients developed SIRS, DIC, and shock within 14 hours of symptom detection.
- Brain death occurred between 16 hours and 4 days after initial symptoms, despite treatments like high-dose steroids and targeted temperature management initiated 3.5-14 hours post-onset.
Conclusions:
- This study provides a detailed temporal map of clinical events and laboratory findings in fatal pediatric AE.
- The rapid onset of systemic complications highlights the aggressive nature of fatal AE and the need for prompt recognition and management.
- Understanding this timeline is vital for future research and clinical strategies aimed at improving outcomes in severe pediatric encephalopathy.
Objective:
Although the mortality among previously healthy children with acute encephalopathy (AE) is approximately 5%, their detailed clinical course has not been clarified. The objective of the present study was to describe the detailed clinical course, in minutes, of fatal AE.
Methods:
We retrospectively reviewed the medical records of five patients (from 6 months to 14 years of age) who previously had no neurological disorders and were diagnosed with brain death due to AE between 2002 and 2018 at Kobe Children's Hospital.
Results:
The initial clinical symptoms were convulsion in three cases and impaired consciousness in two. The earliest noted brain imaging abnormality was 7.5 h after neurological symptom detection. Liver enzymes and creatinine levels increased at initial examination, and sodium elevated gradually. All patients met the criteria of systemic inflammatory response syndrome, disseminated intravascular coagulation, and shock within 14 h of symptom detection. High dose steroids and targeted temperature management were initiated 3.5-14 h after onset. Despite these therapies, patients were diagnosed with brain death from 16 h to 4 days after initial neurological symptoms. AE diagnoses were made between 4 h 29 min and 4 days after initial neurological symptoms and included hemorrhagic shock and encephalopathy syndromes, Reye-like syndrome, and acute necrotizing encephalopathy in two, two, and one patient(s), respectively.
Conclusions:
We revealed the time series' of clinical events (e.g. SIRS, shock, DIC, AE diagnosis, brain death, and treatments) and laboratory findings relative to initial neurological symptom in fatal AE.
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