Haemorrhage, hypercoagulability and ischaemia: Evolution of brain injury after aneurysmal subarachnoid haemorrhage

Aneurysmal subarachnoid haemorrhage (aSAH) is a catastrophic cerebrovascular event associated with high early mortality and substantial long-term disability. Delayed cerebral ischaemia (DCI) is among its most severe complications and a principal driver of secondary neurological injury. Despite decades of research describing diverse pathophysiological mechanisms, a unifying framework for DCI pathogenesis is still lacking, and its clinical prediction remains challenging. We therefore conducted a narrative review to synthesise current understanding of the spatiotemporal evolution of brain injury following aSAH, with emphasis on integrating mechanisms across overlapping clinical phases. Acute phase events from physical effects of bleeding, including intracranial pressure elevation, hyperacute vasospasm and microvascular thrombosis, sets off the evolution of downstream brain injuries. During the early phase, converging mechanisms such as neuroinflammation, oxidative stress, spreading depolarisation and blood-brain barrier disruption coalesce into pan-vascular dysfunction and systemic hypercoagulability. Rather than representing a singular vasospastic complication, these processes collectively evolve into pathobiological states characterised by large-artery vasospasm, microvascular constriction, diffuse capillary occlusion and supply-demand mismatch, ultimately precipitating DCI and cortical infarction. This review examines the key mechanisms underlying these aforementioned processes and aims to establish mechanistic continuity across the evolving phases of injury following aSAH.