Association of hypocapnia in children with febrile seizures

Abstract

Introduction: Febrile seizure is a benign condition in children. Susceptibility genes associated with febrile convulsions have been identified, but the precise pathophysiologic mechanism that triggers febrile seizure is unclear. Using animal models, it has been demonstrated that hyperthermia causes respiratory alkalosis with consequent brain alkalosis and seizures. This study was conducted to find out any association of febrile seizures with fever induced hypocapnia. Methods: We conducted a cross sectional observational study and enrolled 45 children presenting with febrile seizures. Axillary temperature was measured and venous blood gas analysis was done soon after admission and within 24 hour of seizure onset. Mean pH and pCO2 from venous blood gas analysis was measured and compared with standard normal values. Data was analyzed using SPSS software version 17.0 software. Results: The mean pCO2 (27.95 ± 5.31mmHg) was much below normal range, and 91 of children had hypocapnia (pCO2 35) after the febrile seizures. However alkalosis (pH > 7.45) was demonstrated in only 20 of children. Also pCO2 levels in samples drawn before 2 hours were significantly less than those taken after 2 hours (23.24 ± 3.44 vs 29.29 ± 4.99 respectively; p < 0.001). Conclusion: Our data indicates that febrile seizures may be associated with fever induced hyperventilation and ensuing hypocapnia may be one of the precipitating factor in inducing seizures. However, well-structured human trials are needed to demonstrate the same.