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Analysis of Fulminant Cerebral Edema in Acute Pediatric Encephalitis
Shih-Yun Lan1, Jainn-Jim Lin2, Shao-Hsuan Hsia3
1Division of Pediatric Neurology, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan; Chang Gung Children's Hospital Study Group for Children with Encephalitis/Encephalopathy Related Status Epilepticus and Epilepsy (CHEESE), Taoyuan, Taiwan.
Insights
Acute pediatric encephalitis can lead to severe outcomes. Seizures and status epilepticus significantly increase the risk of fulminant cerebral edema in children with this condition.
Area of Science:
- Pediatric Neurology
- Critical Care Medicine
- Infectious Diseases
Background:
- Acute pediatric encephalitis poses a severe threat, potentially leading to rapid fatality or lasting neurological damage.
- Fulminant cerebral edema is a critical complication of pediatric encephalitis.
Purpose of the Study:
- To identify risk factors associated with fulminant cerebral edema in pediatric encephalitis.
- To investigate the role of seizures and status epilepticus in the development of severe cerebral edema.
Main Methods:
- Retrospective review of 1038 pediatric encephalitis cases diagnosed between 2000 and 2010.
- Comparison of risk factors, specifically seizures and status epilepticus, between patients with and without fulminant cerebral edema.
Main Results:
- Among 25 patients with fulminant cerebral edema, 76% experienced seizures and 48% developed status epilepticus prior to edema.
- Seizures and status epilepticus were significantly more prevalent in the fulminant cerebral edema group compared to controls.
- Mortality was high (16 deaths), and no survivors fully recovered.
Conclusions:
- Preceding seizures and status epilepticus are identified as significant risk factors for developing fulminant cerebral edema in acute pediatric encephalitis.
- Early recognition and management of seizures may be crucial in preventing severe outcomes.
Background:
Acute pediatric encephalitis with fulminant cerebral edema can rapidly become fatal or result in devastating neurological sequelae.
Methods:
All cases coded with the discharge diagnosis of acute encephalitis between January 2000 and December 2010 were reviewed. Of the 1038 children with acute pediatric encephalitis, 25 were enrolled in our study with ages ranging from 5 months to 16 years.
Results:
The major neurological symptoms included an altered level of consciousness (72%), vomiting (60%), and headache (48%). The onset of neurological symptoms to signs of brain herniation ranged from 0 days to 9 days. Nineteen (76%) patients had a seizure 24-48 hours prior to showing signs of fulminant cerebral edema, and 12 (48%) patients developed status epilepticus. Sixteen patients died, and no survivors returned to baseline. Risk factors for seizures and status epilepticus were compared between the fulminant cerebral edema group (n = 25, 19 seizures, including 12 status epilepticus) and control group (nonfulminant cerebral edema) (n = 1013, 444 seizures, including 141 status epilepticus; p = 0.001 for seizures and p < 0.001 for status epilepticus).
Conclusion:
Our findings indicate that preceding seizures and status epilepticus are significant risk factors for fulminant cerebral edema in children with acute encephalitis.
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