Elevated intracranial pressure (ICP) is a well-recognized phenomenon in aneurysmal subarachnoid hemorrhage (aSAH) that has been demonstrated to lead to poor outcomes. Despite significant advances in clinical research into aSAH, there are no consensus guidelines devoted specifically to the management of elevated ICP in the setting of aSAH. To treat high ICP in aSAH, most centers extrapolate their treatment algorithms from studies and published guidelines for traumatic brain injury. Herein, the authors review the current management strategies for treating raised ICP within the aSAH population, emphasize key differences from the traumatic brain injury population, and highlight potential directions for future research in this controversial topic.
Naif M. Alotaibi, Justin Z. Wang, Christopher R. Pasarikovski, Daipayan Guha, Fawaz Al-Mufti, Muhammad Mamdani, Gustavo Saposnik, Tom A. Schweizer and R. Loch Macdonald
Christopher R. Pasarikovski, Joel Ramjist, Leodante da Costa, Sandra E. Black and Victor Yang
Studies evaluating individuals for endothelial injury after endovascular thrombectomy (EVT) have been done by means of retrieved human thrombus, MR vessel-wall imaging, and animal histopathological studies. These techniques have limitations, because MR imaging has insufficient spatial resolution to directly visualize endothelium, and histopathological examinations are performed ex vivo and are unable to provide real-time patterns of injury. The purpose of the current study was to obtain in vivo intraluminal imaging after EVT by using optical coherence tomography (OCT), examining for evidence of endothelial injury in real time.
Three consecutive patients with acute basilar artery occlusion underwent OCT imaging immediately after EVT. There were no complications and adequate images were obtained for all patients. Anatomical features of the vessel wall were discernible, including intima, media, adventitia, and internal/external elastic lamina. Basilar artery thick concentric plaque fibrosis was present, causing outward remodeling and loss of the internal/external lamina in certain regions. Evidence of significant residual thrombus was also visible, with mostly red thrombus present despite complete angiographic revascularization. The residual thrombus was not visible on CT, MR, or cerebral angiography and could certainly cause ongoing function-limiting strokes with occlusion of adjacent vital basilar perforators after EVT.