Induced Hypertension in Preventing Cerebral Infarction in Delayed Cerebral Ischemia After Subarachnoid Hemorrhage

Abstract

Background and Purpose— Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage. If clinical signs of DCI occur, induced hypertension is a plausible but unproven therapeutic intervention. There is clinical equipoise if the use of hypertension induction is useful or not with the consequence that this strategy is irregularly used. We explored the effect of blood pressure augmentation in preventing cerebral infarction in patients with clinical signs of DCI. Methods— We performed a retrospective observational study, totaling 1647 patients with aneurysmal subarachnoid hemorrhage admitted at 3 academic hospitals in the Netherlands between 2006 and 2015. To study the primary outcome DCI related cerebral infarcts, we only included patients with no cerebral infarct at the time of onset of clinical signs of DCI. Cox regression was used to test the association between induced hypertension after onset of clinical signs of DCI and the occurrence of DCI related cerebral infarcts. Logistic regression was used to relate hypertension induction with poor outcome after 3 months, defined as a modified Rankin score >3. Results were adjusted for treatment center and baseline characteristics. Results— Clinical signs of DCI occurred in 479 (29%) patients of whom 300 without cerebral infarction on computed tomography scan at that time. Of these 300 patients, 201 (67%) were treated with hypertension induction and 99 were not. Of the patients treated with hypertension induction, 41 (20%) developed a DCI related cerebral infarct compared with 33 (33%) with no induced hypertension: adjusted hazard ratio, 0.59; 95% CI, 0.35 to 0.99. Hypertension induction also prevented poor outcome: adjusted odds ratio, 0.27; 95% CI, 0.14 to 0.55. Conclusions— Hypertension induction seems an effective strategy for preventing DCI related cerebral infarcts if not already present at the time of onset of clinical signs of DCI. This may lead to a reduction in poor clinical outcome.

Contemporary Management of Aneurysmal Subarachnoid Hemorrhage: A Literature Review

“…39 In the induced hypertension group, 20% of patients developed infarcts compared with 33% in the group who did not receive therapy. 39 Unfortunately, an RCT that may have provided additional support was terminated early, due to slow recruitment and a lack of effect on cerebral perfusion. 50 It is an accepted practice that if DCI fails to improve with blood pressure augmentation, trial of an inotropic drug may be acceptable.…”

“…1 The process of DCI is not fully understood but is believed to occur at the cellular and microcirculatory levels, culminating in reduction in blood flow and tissue ischemia or infarction. 39…”

“…29,46,47 Of the components, hypertensive therapy has the most supporting evidence. 27,39,48,49 A recent retrospective observational study of 300 patients with DCI found that hypertensive therapy was associated with a reduction in both cerebral infarcts and poor clinical outcomes. 39 In the induced hypertension group, 20% of patients developed infarcts compared with 33% in the group who did not receive therapy.…”

“…27,39,48,49 A recent retrospective observational study of 300 patients with DCI found that hypertensive therapy was associated with a reduction in both cerebral infarcts and poor clinical outcomes. 39 In the induced hypertension group, 20% of patients developed infarcts compared with 33% in the group who did not receive therapy. 39 Unfortunately, an RCT that may have provided additional support was terminated early, due to slow recruitment and a lack of effect on cerebral perfusion.…”

Symptomatic Cerebral Vasospasm after Spontaneous Subarachnoid Hemorrhage: Comparison of Single and Multiple Intra-arterial Treatment with Respect to the Functional Outcome

“…Treatment options for sCVS, in addition to systemic oral calcium channel antagonists and hemodynamic therapy, 10 consist of local endovascular application of spasmolytic drugs and balloon angioplasty. 11,12 In general, several studies discussed the efficacy of endovascular interventions in patients with sCVS after sSAH, 13 but the use and potential benefit of multiple intraarterial treatments (IATs) in patients with sCVS has to date only been investigated in small case series.…”