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[Herpes simplex encephalitis in childhood]
B Schlüter1, G G Aguigah, G E Bürk
1Neuropädiatrische Abteilung der Vestischen Kinderklinik, Datteln.
Insights
Early acyclovir treatment for herpes simplex encephalitis (HSE) in children is crucial. Prompt antiviral therapy, even before serological confirmation, can improve outcomes in pediatric HSE cases.
Area of Science:
- Pediatric Neurology
- Infectious Diseases
- Virology
Background:
- Herpes simplex encephalitis (HSE) is a severe neurological condition in children.
- Diagnosis and timely treatment are critical for patient outcomes.
Observation:
- This report details the diagnostic and therapeutic experience with 6 pediatric patients (3 weeks to 6.3 years) suffering from HSE.
- Clinical presentations included fever, drowsiness, and seizures.
- Brain imaging (CT scan) and serological tests (IgM-specific HSV antibodies) were used for diagnosis.
Findings:
- Acyclovir therapy was initiated at various stages of illness, from day 4 to day 17.
- Four children treated with acyclovir survived but had severe neurological sequelae.
- Two children, treated with acyclovir on day 7, survived without apparent defects, presenting with tongue vesicles initially.
- One patient experienced a relapse of encephalitis 5 weeks after initial treatment.
Implications:
- HSE should be suspected in children with characteristic symptoms like fever, drowsiness, and seizures.
- Antiviral therapy with acyclovir should be initiated promptly, without solely relying on serological findings.
- Early intervention may influence the severity of neurological sequelae in pediatric HSE.
Abstract:
This is a report on diagnostic and therapeutic experience in 6 patients aged 3 weeks to 6.3 years suffering from herpes simplex encephalitis. In 2 patients, a 3-week-old newborn and a 1.3-year-old boy, acyclovir-therapy started at days 8 and 17 respectively, following the demonstration of hemorrhagic necrosis in the brain by cranial CT-scan and IgM-specific HSV-antibodies in the blood. A 6.3-year-old girl was treated with acyclovir at day 10 of her illness, when cCT showed hemorrhagic necrosis in the brain. It was not before the 21st day, that diagnosis of HSE could be confirmed serologically. She suffered a relapse of encephalitis 5 weeks later. In a 3-month-old boy, treated with acyclovir at day 4 of his illness, IgM-specific HSV-antibodies were found already at day 4. His clinical course was complicated by subdural effusion. These 4 children survived with severe neurologic sequelae. Another 2 patients, a 5- and 7.5-month-old boy respectively, survived without apparent defect. In both cases vesicles upon the tongue appeared in the beginning of illness. Acyclovir-therapy started at day 7, diagnosis being confirmed serologically later. In our experience HSE should be suspected in children suffering from fever, drowsiness and focal or secondarily generalizing seizures. In these cases antiviral therapy should not depend on serologic findings.