Status epilepticus (SE) is a lethal, life-threatening neurologic emergency associated with high levels of morbidity and mortality.1-3 International treatment guidelines recommend the use of benzodiazepines as first-line treatment followed by non-anaesthetic antiseizure drugs as second-line treatment for persistent seizures.4,5 If SE continues, artificial coma induction is usually regarded as the third-line of treatment,6 even though some studies revealed several complications from deep anaesthesia.7-12 However, the lack of treatment options in patients with ongoing SE refractory to antiseizure drugs usually dictates the use of artificial coma induction as a common treatment form in those patients.6 The inconsistent results from past studies, the limited treatment options for refractory SE, and the varied timing of artificial coma induction across medical centres call for further investigation of artificial coma induction.6,13 De Stefano et al. retrospectively evaluated the safety and efficacy of artificial coma induction to treat SE as a second-line treatment option in 230 adult patients.6 The study patients had been treated for SE at 2 Swiss academic medical centres in Geneva and Basel from January 2017 to December 2018.6
Benefits and complications of direct and early artificial coma induction
Direct and early artificial coma induction was associated with shorter SE duration and intensive care unit (ICU) and hospital stays compared with patients who received other treatments.6 Patients receiving this more aggressive treatment had better outcomes than patients who received artificial coma induction after failing treatment with a second-line
non-anaesthetic antiseizure medication.6 Furthermore, complications during SE and outcomes were similar for patients treated with direct and early artificial coma induction after first-line treatment and patients that received treatment escalation according to the guidelines.6 In particular, premorbid neurologic function at hospital discharge was not significantly different and in-hospital death was identical for these two groups.6 De Stefano et al. showed that direct and early artificial coma induction was associated with positive patient outcomes without increasing complications.6 However, these results should be interpreted with caution because of the limited sample sizes for each group.6
In which patient population should direct and early artificial coma induction be considered?
Univariable and multivariate analysis revealed that patients who received direct and early artificial coma induction were younger, more frequently male, had presented with more convulsions and had more severe SE as quantified by the Status Epilepticus Severity Score.6 Subgroup analyses revealed a significant interaction in patients with presumed fatal aetiologies being an additional risk factor for no return to premorbid function compared to patients without presumed fatal aetiologies.6 The differences observed in shorter SE duration and ICU and hospital stays for patients treated with direct and early artificial coma induction could not be explained by differences in comorbidity index or sex alone.6 De Stefano et al. showed that patients with SE could safely benefit from direct and early artificial coma induction.6
A potential answer for those with refractory SE
Prior clinical trials have investigated an aggressive approach to treat patients with SE refractory to first-line benzodiazepine treatment with inconsistent results.7-12 De Stefano et al. presented that direct and early artificial coma induction can significantly reduce the duration of SE and the length of ICU and hospital stays without leading to more complications.6 This study suggests that direct and early artificial coma induction could be a safe option in patients with SE refractory to current first-line treatment options.6
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- Sutter R et al. Nat Rev Neurol. 2016;12(5):281-293.
- Sutter R et al. Epilepsia. 2013;54(3):502-511.
- Brophy GM et al. Neurocrit Care. 2012;17(1):3-23.
- Glauser T et al. Epilepsy Curr. 2016;16(1):48-61.
- De Stefano P et al. 2021;97:e564–e576.
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- Sutter R et al. CNS Drugs. 2017;31(1):65-74.
- Sutter R et al. Neurology. 2014;82(8):656-664.
- Sutter R et al, Epilepsy Behav. 2015;49:294-297.
- Opic P et al. J Clin Neurophysiol. 2020;37(5):399-405.
- Alvarez V et al. Neurology. 2016;87(16):1650-1659.