The evolution of invasive cerebral vasospasm treatment in patients with spontaneous subarachnoid hemorrhage and delayed cerebral ischemia—continuous selective intracarotid nimodipine therapy in awake patients without sedation

Abstract

Cerebral vasospasm (CV) and delayed cerebral ischemia (DCI) are major factors that limit good outcome in patients with spontaneous subarachnoid hemorrhage (SAH). Continuous therapy with intra-arterial calcium channel blockers has been introduced as a new step in the invasive treatment cascade of CV and DCI. Sedation is routinely necessary for this procedure. We report about the feasibility to apply this therapy in awake compliant patients without intubation and sedation. Out of 67 patients with invasive endovascular treatment of cerebral vasospasm due to spontaneous SAH, 5 patients underwent continuous superselective intracarotid nimodipine therapy without intubation and sedation. Complications, neurological improvement, and outcome at discharge were summarized. Very good outcome was achieved in all 5 patients. The Barthel scale was 100 and the modified Rankin scale 0-1 in all cases at discharge. We found no severe complications and excellent neurological monitoring was possible in all cases due to patients' alert status. Symptoms of DCI resolved within 24 h in all 5 cases. We could demonstrate the feasibility and safety of selective intracarotid arterial nimodipine treatment in awake, compliant patients with spontaneous SAH and symptomatic CV and DCI. Using this method, an excellent monitoring of neurological function as well as early detection of other complications is possible. It might be an important step in the risk reduction of invasive CV therapy to improve the outcome with CV and DCI after SAH in selected patients.

Adverse Events and Complications in Continuous Intra-arterial Nimodipine Infusion Therapy After Aneurysmal Subarachnoid Hemorrhage

“…Delayed cerebral ischemia and CV are common complications in the treatment of SAH with a relevant impact on further outcomes (27,28). CIANI became a more common salvage therapy in patients with therapy-refractory CV and DCI (8,10,11,14,29). Since this invasive treatment method is accompanied by many difficulties, our goal was to compare the treatment result after DCI and refractory CV with the frequency and severity of AEs and complications of CIANI therapy.…”

“…If progressive DCI despite hypertension and intravenous application of nimodipine was suspected, a CT-angiogram and CT-perfusion were performed. In the presence of new infarction or a perfusion delay, defined as a mismatch between reduced mean transit time (MTT) (>4 s) and adequate cerebral blood volume (CBV), DSA, and continuous intra-arterial instead of intravenous infusion of nimodipine via indwelling microcatheters in both internal carotid arteries was indicated (Figure 1) (11). Nimodipine-associated hypotension was defined FIGURE 1 | Treatment pathway of delayed cerebral ischemia and cerebral vasospasm.…”

“…Nimodipine represents the only proven standard treatment regimen to prevent and treat cerebral vasospasm (CV) and DCI (6,7). New salvage therapeutic strategies such as intravenous, intra-arterial, or continuous intra-arterial infusion of calcium channel blockers have been introduced recently in the case of therapy refractory CV and DCI (8)(9)(10)(11). Continuous intra-arterial nimodipine infusion (CIANI) might be beneficial for cerebral perfusion pressure and prolong the vasodilatory effect of calcium channel blockers (12).…”

Therapy Results of Pericallosal Aneurysms: A Retrospective Unicenter Study

“…In the postprocedural phase repeated or even continuous intraarterial nimodipine infusions are suitable to relieve affected patients from symptomatic cerebrovascular vasospasm and to reduce the risk of delayed cerebral infarction. 20 , 21 Smaller endovascular devices offer new treatment options for small and wide-necked aneurysms in peripheral locations. Stent-assisted coiling is challenging in pericallosal arteries due to the small vessel diameter and peripheral location of most PAAs.…”

MicroR-146 protects against rat ischemia-reperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway

“…Clinical data indicate that global cerebral ischemia is a leading cause of mortality worldwide (Müller, et al, 2017;Von der Brelie et al, 2017;Aldakkan et al, 2017). Several mechanisms involve in the pathology of cerebral ischemia reperfusion damage including inflammation, cytotoxicity, oxidative stress, apoptosis and excitotoxicity (Gabriel-Salazar et al, 2018;Liu et al, 2018b;Paľa et al, 2019). Cerebral I/R injury frequently injuries the functional area of brain in the hippocampal CA1 pyramidal layer, which further leads to disorder of central nervous system and homeostasis (Jia et al, 2014).…”