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Aktuelle Neurologie 2012; 39(08): 429-436
DOI: 10.1055/s-0032-1309044
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Status Epilepticus

Status Epilepticus
M. Holtkamp
1   Klinik für Neurologie, Charité – Universitätsmedizin Berlin
› Institutsangaben
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Publikationsverlauf

Publikationsdatum:
17. April 2012 (online)

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Zusammenfassung

Dauert ein epileptischer Anfall jedweder klinischer Form länger als 5 min, sollte dieser als Status epilepticus (SE) unverzüglich antikonvulsiv behandelt werden. Mittel der Wahl ist intravenöses Lorazepam (4–8 mg). Persistiert der SE, werden Levetiracetam, Phenytoin oder Valproat gegeben. Bei jedem dritten Patienten ist die epileptische Aktivität jedoch mit diesen Schritten nicht durchbrochen, man spricht hier von einem refraktären Status epilepticus (RSE). Der komplex-fokale SE führt weder zu aktuten systemischen Komplikationen noch zu chronischen neuronalen Konsequenzen. Daher sollte im weiteren therapeutischen Prozedere eher auf Anästhetika verzichtet werden, der Einsatz weiterer nicht-anästhesierender Substanzen wie – falls noch nicht gegeben – Lacosamid, Levetiracetam, Phenytoin oder Valproat wird empfohlen. Beim generalisiert-konvulsiven SE sollte in dieser Konstellation dagegen wegen des hohen Risikos akuter systemischer Komplikationen (z. B. Tachyarrhythmien) unmittelbar ein Anästhetikum (Midazolam, Propofol oder Thiopental) gegeben werden. Die Dosis dieser Substanzen wird gegen ein EEG Burst-Suppression-Muster (Dauer mindestens 24 h) titriert. Pathophysiologisch führt die anhaltende epileptische Aktivität zu einer Abnahme post-synaptischer GABAA-Rezeptoren und somit zu einer Erosion der GABAergen Inhibition. Je später Antikonvulsiva eingesetzt werden, desto geringer ist deren Effizienz. Andererseits nimmt die Zahl der exzitatorischen NMDA-Rezeptoren beim SE zu. Persistiert der SE nach Gabe der o.g. GABAergen Anästhetika, kann in einem späteren Stadium des SE der NMDA-Rezeptor-Antagonist Ketamin in einigen Fällen noch erfolgreich sein. 2 neuere Studien zeigen, dass Patienten selbst einen prolongierten RSE mit wenig funktionellen Einbußen überleben können. Daher sollten eventuelle therapielimitierende Entscheidungen auf der Basis der Prognose der ursächlichen ZNS-Erkrankung und nicht allein auf der Dauer des SE beruhen.

Abstract

Any epileptic seizure lasting more than 5 min should promptly be treated as status epilepticus (SE) by anticonvulsants. Drug of choice is intravenous lorazepam (4–8 mg). If SE persists, second-line anticonvulsants such as levetiracetam, phenytoin and valproate are administered. In every third patient, epileptic activity further continues, this condition is termed refractory status epilepticus (RSE). Complex-partial SE does neither result in acute systemic complications nor in neuronal long-term consequences. Therefore, anticonvulsant treatment after failure of first- and second-line agents should be based on non-anaesthetising substances including – if not already given second-line – lacosamide, levetiracetam, phenytoin or valproate. Anaesthetics should be avoided if possible, as side-effects may be more harmful than continuing non-convulsive epileptic activity. In contrast, generalised-convulsive SE is associated with a high risk of acute systemic morbidity (e. g. cardial arrhythmias), therefore refractory courses should promptly be treated with anaesthetics (midazolam, propofol or thiopental). After bolus administration, these components are titrated against an EEG burst-suppression-pattern for at least 24 h. Pathophysiologically, prolonged epileptic activity results in a decrease of post-synaptic inhibitory GABAA receptors. The later anticonvulsants are administered, the less likely they terminate epileptic activity. In contrast, excitatory NMDA receptors increase with ongoing SE. Therefore, NMDA receptor antagonists such as ketamine may be efficient in later stages of SE after GABAergic anaesthetics have failed. Recent data demonstrate that even patients with prolonged RSE can survive with favourable functional outcome. Therefore, end-of-life decisions in SE may be based on the expected prognosis of the underlying brain disorder rather than on duration of SE.

Schlüsselwörter

prolongierter Anfall - GABAerge Inhibition - Refraktärität - Prognose

Keywords

prolonged seizure - GABAergic inhibition - refractoriness - prognosis
 

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