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. 2022 Aug 9;11(16):4642.
doi: 10.3390/jcm11164642.

Vasospasm-Related Death after Aneurysmal Subarachnoid Hemorrhage: A Retrospective Case-Control Study

Affiliations

Vasospasm-Related Death after Aneurysmal Subarachnoid Hemorrhage: A Retrospective Case-Control Study

Ali Khanafer et al. J Clin Med. .

Abstract

Background: Vasospasm after the rupture of an intracranial aneurysm is a frequent phenomenon and is the main cause of morbidity and mortality in patients who have survived intracranial hemorrhage and aneurysm treatment. We analyzed the diagnosis and management of patients with aneurysmal subarachnoid hemorrhage who eventually died from ischemic brain damage due to vasospasm.

Methods: Between January 2007 and December 2021 (15 years), a total of 1064 patients were diagnosed with an aneurysmal intracranial hemorrhage in a single comprehensive neurovascular center. Vasospasm was diagnosed in 408 patients (38.4%). A total of 187 patients (17.6%) died within 90 days of the aneurysm rupture. In 64 of these 187 patients (33.7%), vasospasm was considered to be the cause of death. In a retrospective analysis, demographic and clinical data for patients without, with non-fatal, and with fatal vasospasm were compared. The patients with fatal vasospasm were categorized into the following subgroups: "no diagnosis and treatment" (Group a), "delayed diagnosis" (Group b), "cardiovascular complications" (Group c), and "vasospasm-treatment complications" (Group d).

Results: Among the patients with fatal vasospasm, 31 (48.4%) were assigned to group a, 26 (40.6%) to group b, seven (10.9%) to group c, and none (0%) to group d.

Conclusion: The early recognition of severe posthemorrhagic vasospasm is a prerequisite for any treatment and requires routine diagnostic imaging in all unconscious patients. Aggressive endovascular vasospasm treatment may fail to prevent death but is infrequently the cause of a fatal outcome.

Keywords: cerebral vasospasm; endovascular treatment; intracranial aneurysm; subarachnoid hemorrhage.

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Conflict of interest statement

The authors have no conflict of interest in this regard.

Figures

Figure 1
Figure 1
Diagnostic imaging of a 57-year-old male patient with an aSAH due to a ruptured MCA aneurysm. Computed tomography (a) and CTA (b) revealed a massive aSAH and early vasospasm. CCT after one day (c,d) showed large ischemic infarctions.
Figure 2
Figure 2
Diagnostic imaging and EVT in a 70-year-old female patient with an aSAH due to a ruptured basilar artery aneurysm. CT (a) showed a massive aSAH. DSA (b) with contrast-medium injection of the left vertebral artery (VA; lateral projection, asterisk) demonstrated the EVT with the coil mass inside the aneurysm. DSA (c) with contrast-medium injection of the right internal carotid artery (ICA; posterior–anterior projection) revealed massive vasospasm. Post-interventional CT (d) showed ischemic infarctions despite EVT.
Figure 3
Figure 3
Diagnostic imaging and EVT in a 50-year-old female patient with an aSAH due to a ruptured left ICA aneurysm. Cranial CT (a) showed an aSAH. DSA with contrast-medium injection of both hemispheres revealed massive vasospasm (b,c). Post-interventional CT showed ischemic infarctions of both hemispheres (d).
Figure 4
Figure 4
Diagnostic imaging and EVT in a 39-year-old female patient with an aSAH due to a ruptured anterior communicating artery (AcomA) aneurysm. Cranial CT showed an aSAH (a). DSA with a contrast-medium injection of the left ICA artery (lateral view 45°) showed an embolic occlusion of the superior trunk of the left MCA (arrow) and ACA (b) with the dissolution of the thrombus after infusion of rtPA (c). Cranial CT showed massive ischemic infarctions of both ICA and MCA supply territories (d).
Figure 5
Figure 5
Flowchart summarizing the numbers of patients in the different subgroups.

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