Impaired cerebrovascular reactivity may predict delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

Abstract

Introduction: Delayed cerebral ischemia (DCI) is a major cause of disability and death after aneurysmal subarachnoid hemorrhage. The literature suggests that impaired cerebrovascular reactivity (CVR) may be a predictor for DCI; still no CVR based prediction model has been developed. Increased knowledge about possible predictors of DCI can improve patient management in high-risk patients and allow for shorter hospital stay in low-risk patients. Method: CVR was examined in 42 patients with aneurysmal subarachnoid hemorrhage and 37 patients treated for unruptured intracranial aneurysm, using acetazolamide test with transcranial Doppler monitoring of blood flow velocities. Patients were followed for development of DCI, separated into clinical deterioration and radiographic infarction. Results: For all patients, regardless of aneurysm rupture status, CVR was on average 5.5 percentage points lower on the ipsilateral side of aneurysm treatment. Patients with clinical deterioration due to DCI had lower CVR than patients without DCI, and the difference was larger on the contralateral side (33.9% vs. 49.2%). Two prediction models were constructed for clinical deterioration due to DCI. The area under the receiver operating characteristic curve was 0.82 in the model using established predictors, and 0.86 in the model that also included CVR. Conclusion:Our findings support the hypothesis that impaired CVR may be an independent predictor of clinical deterioration due to DCI, and may assist in identifying patients at risk after aneurysmal subarachnoid hemorrhage. Ipsilateral CVR reduction occurs in all patients after aneurysm treatment, regardless of DCI development, thus highlighting the need to evaluate ipsi-and contralateral CVR separately.

The Effects of Acetazolamide on Cerebral Hemodynamics in Adult Patients with an Acute Brain Injury: A Systematic Review

“…Acetazolamide was administered intravenously in all studies. The most frequent dose was 1000 mg, given as bolus; different doses were also used, including 500 mg [21], 17 mg/Kg [18], and 1000 mg for body weight < 80 Kgs or 15 mg/kg for body weight > 80 Kgs for a maximum of 1500 mg [22]. In the studies enrolled, no systematic differentiation of the dose according to the pathology analyzed was observed.…”

Effect of hypertension and medication use regularity on postoperative delirium after maxillofacial tumors radical surgery

“…According to relevant literature reports, intraoperative hypotension does not directly cause postoperative delirium [ 17 ], but for patients with different cerebral blood flow regulation [ 18 ], using the same blood pressure maintenance standard will significantly increase the incidence of postoperative POD, which indicates that compared with intraoperative blood pressure, more attention should be paid to the patient’s basic cerebrovascular function and adjustment ability. According to previous research reports, hypertension could impair the cerebrovascular reactivity in older adults, and impaired cerebrovascular reactivity may be a predictor for delayed cerebral ischemia [ 19 ]. This may provide a reasonable explanation for delirium that usually occurs 1 to 2 days after surgery rather than immediately.…”

Defining Optimal Dosing of Nimodipine in Aneurysmal Subarachnoid Hemorrhage: Study Protocol for a Systematic Review

“…Therapeutic dose monitoring strategies (TDM) could optimize nimodipine dosing in these patients. In addition to vasospasm, other processes such as cerebral arterial micro-thrombosis [17], cerebral autoregulation dysfunction, collateral ow dynamics [18] and cortical spread depolarization [19] have shown to contribute to cerebral infarct, independently of vasospasm.…”