Delayed cerebral ischaemia after subarachnoid haemorrhage: pathophysiology, diagnosis and neurotherapeutic opportunities

Delayed cerebral ischaemia is a serious complication following aneurysmal subarachnoid haemorrhage (aSAH), leading to poor outcomes. This review discusses the pathophysiology of DCI, focusing on the role of cerebral vasospasm, reduction in the cerebral blood flow and the factors that affect the vasospasm and DCI. Biomarkers play a crucial role in DCI's recognition, risk stratification, and outcome prediction. Goal-directed management aims to ameliorate the reduced cerebral blood flow, restore circulation and substrate delivery, and protect neurons. These strategies include the maintenance of cerebral blood flow and restoring substrate delivery by optimising oxygenation and maintaining normoglycaemia. Neuroprotective agents, such as calcium channel blockers like nimodipine, play a crucial role by reducing neuronal calcium influx and improving collateral circulation. Multimodal monitoring, incorporating techniques like transcranial Doppler, continuous EEG, and intracranial pressure monitoring, is essential for guiding treatment decisions and evaluating the efficacy of interventions. In the future, research should focus on a comprehensive approach to DCI management with pharmacological interventions and individualised treatment strategies.