Impairment of Cerebral Perfusion and Infarct Patterns Attributable to Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Weidauer, Stefan; Lanfermann, Heinrich; Raabe, Andreas; Zanella, Friedhelm E.; Seifert, Volker; Beck, Jürgen

doi:10.1161/strokeaha.106.477976

Cited by 150 publications

(106 citation statements)

References 34 publications

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“…Regions of both infarction and hemorrhage are also known to develop in the setting of cerebral vasoconstriction or vasospasm. 55,[57][58][59][60] In aneurysmal subarachnoid hemorrhage, early vasospasm can occur with infarction and both petechial blood and focal hematoma formation. 55 In the reversible cerebral vasoconstric-tion syndrome, watershed infarction and focal brain hematomas have been observed, potentially due to reperfusion.…”

Section: Presence Of Hypertensionmentioning

confidence: 99%

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

Hefzy¹,

Bartynski²,

Boardman³

et al. 2009

AJNR Am J Neuroradiol

291

227

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Section: Presence Of Hypertensionmentioning

confidence: 99%

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

Hefzy¹,

Bartynski²,

Boardman³

et al. 2009

AJNR Am J Neuroradiol

291

227

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“…In patients experiencing DCI, positron emission tomographic cerebral perfusion patterns do not correlate with increased blood flow velocities at TCD (Minhas et al, 2003). Finally, patients with SAH may also develop ischemia and cortical band-like infarctions without any evidence of vasospasm (Rabinstein et al, 2004;Naidech et al, 2006;Lee et al, 2006;Weidauer et al, 2007Weidauer et al, , 2008.…”

Section: Introductionmentioning

confidence: 97%

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

Vergouwen

Vermeulen

Coert

et al. 2008

J Cereb Blood Flow Metab

289

195

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Patients with aneurysmal subarachnoid hemorrhage (SAH) who experience delayed cerebral ischemia (DCI) have an increased risk of poor outcome. Delayed cerebral ischemia is considered to be caused by vasospasm. However, not all patients with DCI have vasospasm. Inversely, not all patients with vasospasm develop clinical symptoms and signs of DCI. In the past, treatments aiming at vasospasm were not successful in preventing ischemia. The purpose of this review is to give an overview of clinical data showing that DCI cannot always be attributed to vasospasm, and to present an in-depth analysis of clinical and autopsy studies on the role of microthrombosis in the pathogenesis of DCI. Clinical studies show that DCI is associated with an activation of the coagulation cascade within a few days after SAH, preceding the time window during which vasospasm occurs. Furthermore, impaired fibrinolytic activity, and inflammatory and endotheliumrelated processes, lead to the formation of microthrombi, which ultimately result in DCI. The presence of microthrombi is confirmed by autopsy studies. Insight in the pathophysiology of DCI is crucial for the development of effective therapies against this complication. Because multiple pathways are involved, future research should focus on drugs with pleiotropic effects.

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“…24 For the VIH patients, radiographic vasospasm was mild in 23 patients (13.1%), moderate in 66 patients (37.5%), and severe in 87 patients (49.4%). Radiographic vasospasm involved the anterior circulation in 173 patients (98.3%) and posterior circulation in 32 patients (18.2%).…”

Section: Severity Location and Treatment Of Vasospasmmentioning

confidence: 88%

The safety of vasopressor-induced hypertension in subarachnoid hemorrhage patients with coexisting unruptured, unprotected intracranial aneurysms

Reynolds

Buckley

Indrakanti

et al. 2015

JNS

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obJect Vasopressor-induced hypertension (VIH) is an established treatment for patients with aneurysmal subarachnoid hemorrhage (SAH) who develop vasospasm and delayed cerebral ischemia (DCI). However, the safety of VIH in patients with coincident, unruptured, unprotected intracranial aneurysms is uncertain. methods This retrospective multiinstitutional study identified 1) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who required VIH therapy (VIH group), and 2) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who did not require VIH therapy (non-VIH group). All patients had previously undergone surgical or endovascular treatment for the presumed ruptured aneurysm. Comparisons between the VIH and non-VIH patients were made in terms of the patient characteristics, clinical and radiographic severity of SAH, total number of aneurysms, number of ruptured/unruptured aneurysms, aneurysm location/size, number of unruptured and unprotected aneurysms during VIH, severity of vasospasm, degree of hypervolemia, and degree and duration of VIH therapy. results For the VIH group (n = 176), 484 aneurysms were diagnosed, 231 aneurysms were treated, and 253 unruptured aneurysms were left unprotected during 1293 total days of VIH therapy (5.12 total years of VIH therapy for unruptured, unprotected aneurysms). For the non-VIH group (n = 73), 207 aneurysms were diagnosed, 93 aneurysms were treated, and 114 unruptured aneurysms were left unprotected. For the VIH and non-VIH groups, the mean sizes of the ruptured (7.2 ± 0.3 vs 7.8 ± 0.6 mm, respectively; p = 0.27) and unruptured (3.4 ± 0.2 vs 3.2 ± 0.2 mm, respectively; p = 0.40) aneurysms did not differ. The authors observed 1 new SAH from a previously unruptured, unprotected aneurysm in each group (1 of 176 vs 1 of 73 patients; p = 0.50). Baseline patient characteristics and comorbidities were similar between groups. While the degree of hypervolemia was similar between the VIH and non-VIH patients (fluid balance over the first 10 days of therapy: 3146.2 ± 296.4 vs 2910.5 ± 450.7 ml, respectively; p = 0.67), VIH resulted in a significant increase in mean arterial pressure (mean increase over the first 10 days of therapy relative to baseline: 125.1% ± 1.0% vs 98.2% ± 1.2%, respectively; p < 0.01) and systolic blood pressure (125.6% ± 1.1% vs. 104.1% ± 5.2%, respectively; p < 0.01). coNclusioNs For small, unruptured, unprotected intracranial aneurysms in SAH patients, the frequency of aneurysm rupture during VIH therapy is rare. The authors do not recommend withholding VIH therapy from these patients.

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Impairment of Cerebral Perfusion and Infarct Patterns Attributable to Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Cited by 150 publications

References 34 publications

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

Hemorrhage in Posterior Reversible Encephalopathy Syndrome: Imaging and Clinical Features

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

The safety of vasopressor-induced hypertension in subarachnoid hemorrhage patients with coexisting unruptured, unprotected intracranial aneurysms

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