Abstract
Purpose
Angiographic vasospasm (CVS) has been accused to be the main cause of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH). However, treatment success including endovascular treatment remains to be improved. We performed a pattern analysis of ischemic lesions in SAH patients in the absence of angiographic cerebral vasospasm to generate further hypotheses concerning etiology and risk factors of DCI apart from vasospastic narrowing.
Methods
We retrospectively included 309 patients with cerebral infarcts after SAH. Vasospasm was assessed by means of CT or MR angiography and perfusion measurement or digital subtraction angiography. All clinical and radiological data were used to determine the most probable etiology for new infarcts.
Results
Twenty-seven percent of patients showed infarcts without presence of angiographic vasospasm. Seventy-three percent of these “atypical infarcts” were induced by complications of aneurysm therapy, 7 % by hypoxia, 2 % by ICP-related herniation. In 17 %, the etiology remained unclear; however, disturbances of the microcirculation for different reasons were the most likely cause in these patients.
Conclusion
Beyond CVS and treatment complications, a not insignificant number of SAH patients suffered from infarcts of other etiology probably due to disturbance of the microcirculation. Therapeutic approaches for vasodilation of angiographic vasospasm alone should be reconsidered.
Zusammenfassung
Ziel
Als Ursache verzögert auftretender Infarkte (DCI) nach aneurysmatischer Subarachnoidalblutung (SAB) werden meist angiographisch nachweisbare Vasospasmen (CVS) angenommen. Die Erfolge auch endovaskulärer Therapieansätze des angiographischen Vasospasmus sind jedoch begrenzt. Wir analysierten die Infarktmuster bei Patienten mit aneurysmatischer SAB ohne angiographisch nachweisbare Vasospasmen, um alternative Hypothesen hinsichtlich der Ätiologie und der Risikofaktoren von DCI zu generieren.
Methoden
Dreihundertneun Patienten mit zerebralen Infarkten nach SAB wurden retrospektiv in die Studie eingeschlossen. Das Vorliegen von Vasospasmen wurden durch CT oder MR Angiographie und Perfusionsmessung oder digitale Subtraktionsangiographie untersucht. Alle klinischen und radiologischen Daten wurden verwendet, um die wahrscheinlichste Ätiologie neu aufgetretener Infarkte zu benennen.
Ergebnisse
Siebenundzwanzig Prozent der Patienten zeigten Infarkte ohne Nachweis angiographischer Vasospasmen. Dreiundsiebzig Prozent dieser „atypischen Infarkte“ waren Folge der Aneurysmabehandlung, 7 % einer Hypoxie, 2 % einer Herniation aufgrund erhöhten intrakraniellen Drucks. Bei 17 % der Patienten blieb die Ätiologie unklar, wobei laminäre oder runde kortikale Infarkte angrenzend an subarachnoidale Blutclots als häufigstes Muster zu erkennen waren.
Schlussfolgerung
Neben dem zerebralen Vasospasmus und Komplikationen der Aneurysmatherapie treten nach aneurysmatischer SAB zerebrale Infarkte anderer Ätiologie auf, die wahrscheinlich Folge einer Mikrozirkulationsstörung sind. Zusätzlich zu den ausschließlich auf eine Dilatation der angiographischen Vasospasmen angelegten Therapiekonzepten, deren Behandlungserfolg bisher begrenzt ist, sind vor diesem Hintergrund alternative Therapiekonzepte erforderlich.
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Wagner, M., Steinbeis, P., Güresir, E. et al. Beyond Delayed Cerebral Vasospasm: Infarct Patterns in Patients with Subarachnoid Hemorrhage. Clin Neuroradiol 23, 87–95 (2013). https://doi.org/10.1007/s00062-012-0166-x
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DOI: https://doi.org/10.1007/s00062-012-0166-x
Keywords
- Cerebral vasospasm
- Delayed cerebral ischemia
- Aneurysmal subarachnoid hemorrhage
- Cortical spreading depolarization
- Microcirculation