| Abstract [eng] |
Introduction. Aneurysmal subarachnoid hemorrhage (aSAH) is a severe cerebrovascular pathology characterized by high mortality and disability rates. Even after successful isolation of a ruptured aneurysm, patients remain at high risk for delayed cerebral ischemia (DCI) and cerebral vasospasm. The aim of this work is to conduct a scientific literature review to evaluate the latest pathogenic mechanisms of aSAH-induced vasospasm and to review modern diagnostic and stepwise treatment algorithms. Methods. International medical databases were used for the literature review, analyzing clinical trials, meta-analyses, and AHA/ASA guidelines from the past decade. Literature selection was focused on the complex nature of vasospasm, multimodal neuromonitoring, and escalated treatment. Results. Literature analysis indicates that cerebral vasospasm is no longer treated solely as a myogenic narrowing of large vessels. It is a complex failure of the neurovascular unit, encompassing endothelial dysfunction, microcirculatory impairment, neuroimmune inflammation, and cortical spreading depolarizations (CSD). Clinical assessment or angiography alone is no longer sufficient for early diagnosis; an increasing role is played by computed tomography perfusion (CTP), transcranial Doppler (TCD), multimodal neuromonitoring (cEEG, microdialysis), and artificial intelligence (AI) algorithms. Treatment strategies have evolved from aggressive 3H therapy toward strict maintenance of euvolemia, neuroprotection (nimodipine), and induced hypertension. In cases of refractory vasospasm, endovascular chemical or mechanical angioplasty remains the primary rescue therapy, although the use of systemic vasodilators is limited by the vascular "steal" phenomenon. Conclusions. The management of DCI and vasospasm after aSAH requires a personalized, pathophysiologically grounded approach. Modern diagnostic tools and a stepwise treatment algorithm allow for the timely identification of tissue hypoxia and the application of targeted interventions, thereby reducing the risk of secondary brain injury. |
