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P103 Endovascular therapy for cerebral vasospasm after aneurysmal subarachnoid hemorrhage: single-center experience in a high-volume neurovascular unit
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  1. Julian Schwarting1,2,
  2. Carolin Albrecht3,
  3. Dominik Trost1,
  4. Isabel Hostettler4,
  5. Martin Renz1,
  6. Bernhard Meyer5,
  7. Claus Zimmer1,
  8. Jan Kirschke1,
  9. Christian Maegerlein1,
  10. Jannis Bodden1,
  11. Charlotte Lingg6,
  12. Arthur Wagner5,
  13. Maria Wostrack5,
  14. Tobias Boeckh-Behrens1
  1. 1Department of Diagnostic and Interventional Neuroradiology, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, Munich, Germany
  2. 2Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany
  3. 3Department of Neurosurgery, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, Munich, Germany
  4. 4Department of Neurosurgery, Cantonal Hospital St. Gallen, St. Gallen, Switzerland
  5. 5Department of Neurosurgery, Technical University of Munich, School of Medicine, Klinikum rechts der Isar,, Munich, Germany
  6. 6Department of Anesthesiology, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, Munich, Germany

Abstract

Introduction Subarachnoid hemorrhage (SAH) frequently leads to cerebral vasospasms (CVS) of large cerebral arteries as part of delayed cerebral ischemia (DCI). Endovascular treatment of CVS by local intraarterial application of calcium antagonists or mechanical dilatation of focal stenoses has become an additional therapeutic option in selected cases; its relevance for clinical practice remains controversial.

Aim of Study To examine the potential benefits of endovascular intervention for the treatment of CVS following SAH.

Methods In a retrospective monocentric cohort study, we included 310 SAH patients developing CVS during the hospital stay and evaluated their clinical and radiographic outcomes. Severe vasospasm was defined by a mean velocity of >200 cm/sec in transcranial Doppler ultrasound and/or occurrence of new neurological deficits and/or decrease of at least 2 points on the Glasgow Coma Scale (GCS), respectively.

Results 92 patients (29.7%) underwent endovascular interventions due to persistent symptoms despite conservative therapy. Among endovascularly treated patients, 86% (n=79) improved in terms of angiographic results. 71% (n = 44) who underwent endovascular interventions due to symptomatic deterioration improved clinically. Clinical worsening occurred in 18% of cases (n=11). Periprocedural complications were observed in 4% (n=4).

Conclusion Endovascular intervention emerges as a safe and effective therapy for individuals experiencing delayed ischemic neurologic deficits triggered by large-artery vasospasm following SAH. Embedded in a standardized detection and medical management process and coupled with well-defined criteria for endovascular interventions, it is an efficient preventative approach to enhance neurological outcomes after SAH.

Disclosure of Interest no.

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