Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage

Abstract

Background: Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14. Methods: We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both. Results: Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH-Physiologic Derangement Score (PDS) .2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH-PDS than patients with later cerebral infarction (p = 0.025). Conclusions : Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.

Endovascular options in the treatment of delayed ischemic neurological deficits due to cerebral vasospasm

“…Our initial management option is to optimize medical therapy, primarily through hyperdynamic therapy. 26,32 The patient's neurological examination or assessment parameters are closely followed. If the patient improves and can tolerate medical therapy, it is continued.…”

“…22 Once the aneurysm is secured, more aggressive forms of medical management are typically instituted after a spasm is diagnosed, such as triple-H therapy, or hyperdynamic therapy without intentional anemia. 26,32 Triple-H therapy improves cerebral perfusion and can improve clinical outcomes, 17,24,44,48 but it has not been definitively shown to prevent cerebral vasospasm. 24,29 The prophylactic use of triple-H therapy is typically not indicated.…”

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

“…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.…”

Dissociation of Early and Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

“…Cerebral infarction after aSAH is common [1][2][3] and can be classified as early or delayed. Infarction may occur as early brain injury because of initial aneurysm rupture, [4][5][6] or as delayed cerebral ischemia, 7 often attributed to arterial vasospasm. 5,8,9 Increasingly, evidence also points to infarction as a result of iatrogenic injury caused by either neurosurgical clipping 2,8 or endovascular coiling.…”