Management of delayed cerebral ischemia after subarachnoid hemorrhage

Abstract

For patients who survive the initial bleeding event of a ruptured brain aneurysm, delayed cerebral ischemia (DCI) is one of the most important causes of mortality and poor neurological outcome. New insights in the last decade have led to an important paradigm shift in the understanding of DCI pathogenesis. Large-vessel cerebral vasospasm has been challenged as the sole causal mechanism; new hypotheses now focus on the early brain injury, microcirculatory dysfunction, impaired autoregulation, and spreading depolarization. Prevention of DCI primarily relies on nimodipine administration and optimization of blood volume and cardiac performance. Neurological monitoring is essential for early DCI detection and intervention. Serial clinical examination combined with intermittent transcranial Doppler ultrasonography and CT angiography (with or without perfusion) is the most commonly used monitoring paradigm, and usually suffices in good grade patients. By contrast, poor grade patients (WFNS grades 4 and 5) require more advanced monitoring because stupor and coma reduce sensitivity to the effects of ischemia. Greater reliance on CT perfusion imaging, continuous electroencephalography, and invasive brain multimodality monitoring are potential strategies to improve situational awareness as it relates to detecting DCI. Pharmacologically-induced hypertension combined with volume is the established first-line therapy for DCI; a good clinical response with reversal of the presenting deficit occurs in 70 % of patients. Medically refractory DCI, defined as failure to respond adequately to these measures, should trigger step-wise escalation of rescue therapy. Level 1 rescue therapy consists of cardiac output optimization, hemoglobin optimization, and endovascular intervention, including angioplasty and intra-arterial vasodilator infusion. In highly refractory cases, level 2 rescue therapies are also considered, none of which have been validated. This review provides an overview of current state-of-the-art care for DCI management.

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

“…To alleviate SAH-induced CV, a number of medications have been tested in clinic and laboratory. Nimodipine, a dihydropyridine calcium channel blocker, is the most widely used and the only effective pharmacologic intervention to prevent and cure CV in practice (Francoeur & Mayer, 2016). Nonetheless, there was no definite connection with angiographic alleviation and functional improvement (Laskowitz & Kolls, 2010).…”

Can Levosimendan Be a Treatment Option in Subarachnoid Hemorrhage?

“…Hipotansiyon ve hipovolemi, lokal serebral kan akımını azaltır ve bu da gecikmiş serebral iskemi riskinde artışa neden olur (19). Serebral vazospazm tedavisinde "triple-H" (hipertansif, hipervolemik, hemodilüsyon) tedavisi uzun yılladır bilinmektedir (20). Hipervolemi ve hemodilüsyon, "triple-H" tedavisinin tartışmalı kısımları olmakla birlikte teorik olarak hacim genişlemesiyle elde edilen hemodilüsyon, kalp debisini artırarak kalp dolum basınçlarını, kan basıncını ve serebral kan akımını artırabilir ve serebral iskemiyi önleyebilir (21).…”

Automated Grading of Cerebral Vasospasm to Standardize Computed Tomography Angiography Examinations After Subarachnoid Hemorrhage

“…Of the patients who survive the initial bleeding event, up to 30% then suffer delayed cerebral ischemia (DCI) during the first weeks after SAH (4,5). DCI is defined as a new global or focal neurological impairment that lasts for at least 1 h or a new cerebral infarction that was not immediately apparent after aneurysm occlusion and which is attributable to ischemia and not to other causes (6). The underlying pathophysiology of DCI is only partially understood.…”

“…The underlying pathophysiology of DCI is only partially understood. However, it is accepted that its genesis is multifactorial, with factors including vasospasms of the large intracranial arteries, disturbance of the microcirculation by vasospasms and the microthrombosis of microvessels, cortical spreading depression, and inflammatory effects (4)(5)(6)(7).…”