Latar belakang: Status epileptikus non-konvulsivus (SENK) dapat terjadi setelah status epileptikus konvulsivus (SEK). SENK yang terjadi pasca-SEK memiliki mortalitas sebesar 34,9%. Sehingga, pada keadaan penurunan kesadaran pasca-SEK harus dicurigai suatu SENK yang dibuktikan dengan pemeriksaan elektroensefalografi (EEG) untuk menegakkan diagnosis agar luaran pasien menjadi lebih baik. Penelitian ini bertujuan untuk mengetahui insiden SENK pasca-SEK dan faktor-faktor yang mempengaruhinya.
Metode Penelitian: Penelitian ini menggunakan desain potong lintang menggunakan data sekunder. Sampel di ambil dengan metode total sampling yaitu pada subjek yang mengalami penurunan kesadaran pasca-SEK dari bulan Maret 2019-Oktober 2020 di Rumah Sakit Dokter Cipto Mangunkusumo (RSUPN Dr. Cipto mangunkusumo) Jakarta. Penegakan diagnosis SENK menggunakan EEG dengan kriteria modified salzburg consensus criteria for non-convulsive status epilepticus (mSCNC)
Hasil Penelitian: Sebanyak 74 subjek mengalami penurunan kesadaran pasca-SEK. Median usia 46 (18-80) tahun dengan dominasi perempuan. Median frekuensi bangkitan epileptik saat SEK sebanyak 4(1-30) kali, SEK terjadi selama 1-5 menit pada 73% subjek. Median derajat kesadaran pasca SEK skala koma Glasgow (SKG) 11(5-14). Etiologi tersering adalah intrakranial (66,2%) yang terjadi akut (71,6%) akibat iskemia otak (20,3%). Riwayat epilepsi didapatkan pada 36,5% subjek. Insiden SENK dari Maret 2019 – Oktober 2020 sebesar 33,8%. Berdasarkan kriteria mSCNC, SENK definit 24%, sebesar 12% masing-masing berupa bangkitan epileptiform > 2,5Hz dan aktivitas ritmik disertai evolusi spasiotemporal. Sementara possible SENK 56% dengan gambaran tersering berupa aktivitas ritmik tanpa fluktuasi. Pada subjek yang tidak SENK didapatkan gambaran EEG abnormal sebanyak 87,3% dengan gambaran nonepileptiform berupa perlambatan (71,4%). Tidak terdapat perbedaan demogarafi dan klinis bermakna pada kedua kelompok, namun pada kelompok SENK didapatkan median usia lebih tua (52 vs 44 tahun). Sedangkan pada kelompok tidak SENK, lebih banyak didapatkan riwayat epilepsi (44,9%) dibandingkan kelompok SENK (20%) (p = 0,035). Analisa multivariat menunjukkan risiko mengalami SENK saat tidak memiliki riwayat epilepsi adalah sebesar 3.259 kali (p = 0,040; IK95% 1,053-10,091).
Kesimpulan: Insiden SENK didapatkan sebesar 33,8%. Berdasarkan kriteria mSCNC, definit 24%, sebesar 12% masing-masing berupa bangkitan epileptiform > 2,5Hz dan aktivitas ritmik disertai evolusi spasiotemporal. Sementara possible SENK 56% dengan gambaran tersering berupa aktivitas ritmik tanpa fluktuasi. Pasien tanpa riwayat epilepsi, memiliki resiko sebesar 3,259 kali mengalami SENK pasca-SEK.
Background: Nonconvulsive status epilepticus (NCSE) may occur following convulsive status epilepticus (CSE), with the mortality rate of 34.9%. Therefore, in persistent loss of consciousness following CSE, NCSE must be considered and electroencephalography (EEG) should be performed to ensure the diagnosis and improve the outcome. This study aimed to describe the incidence of NCSE following CSE and its associated factors. Methods: This was a cross-sectional study using secondary data of every subjects with loss of consciousness following CSE from March 2019 to October 2020 in Cipto Mangunkusumo National General Hospital, Jakarta. The diagnosis of NCSE was performed using modified Salzburg consensus criteria for non-convulsive status epilepticus (mSCNC). Results: There were 74 subjects with loss of consciousness following CSE. The median age of 46 (18-80) years predominantly female. The median frequency of seizure at CSE was 4 (1-30) times and occurred for 1-5 minutes in 73% of subject. The median degree of consciousness following CSE Glasgow Coma Scale (GCS) 11 (5-14). The most common etiology was related to intracranial etiology (66.2%) that occurs in acute (71,6%) due to cerebral ischemia (20.3%). A history of epilepsy was found in 36.5% subject The incidence of NCSE from March 2019 to October 2020 was 33.8%. Based on mSCNC criteria, the definite NCSE was 24%, 12% respectively was epileptiform discharge >2.5 Hz and rhythmic activity with spasiotemporal evolution. The possible NCSE was 56 % with the most common EEG finding was rhythmic activity without fluctuation. In group NCSE, there was abnormal EEG 87.3% with non-epileptiform in form of slowing. There were no significant demographic and clinical differences in two group, but in NCSE group the median age was older (52 vs 44 years). Meanwhile, in the non NSCE group, there was more history of epilepsy (44.9) than NCSE group (20%) (p=0.035). Multivariate analysis showed the risk of NCSE when no history of epilepsy was 3.259 times (p = 0,040; IK95% 1,053-10,091). Conclusion: The incidence of NCSE following CSE was 33.8%. Based on mSCNC criteria, the definite NCSE was 24%, 12% respectively was epileptiform discharge >2.5 Hz and rhythmic activity with spasiotemporal evolution. The possible NCSE was 56 % with the most common EEG finding was rhythmic activity without fluctuation. Subjects without history of epilepsy had 3.259 higher risk to develop NCSE following CSE.