Abstract Introduction Cerebral vasospasm (CVS) is an often overlooked complication of ruptured arteriovenous malformations (AVMs), despite its occurrence in approximately 13% of cases. This secondary insult can lead to delayed cerebral ischemia (DCI) and high morbidity, and its management is challenging without specific treatment guidelines. The pathophysiology of post-AVM vasospasm appears to differ from that of aneurysmal subarachnoid hemorrhage (aSAH) - likely involving prolonged intraventricular blood stasis and endothelial dysfunction. We present a four-patient case series of refractory CVS after ruptured AVMs to underscore the clinical importance of early identification, intensive care monitoring, and tailored management of this complication. Case Description Four patients with ruptured supratentorial AVMs developed CVS in the postoperative period following surgical treatment. In the neurologic intensive care unit, daily transcranial Doppler (TCD) monitoring - including Lindegaard index tracking - enabled early detection of vasospasm. Elevations in cerebral blood flow velocity prompted aggressive medical management with induced hypertension and intravenous milrinone. Despite these measures, refractory vasospasm persisted, necessitating endovascular rescue therapy. All four patients underwent balloon angioplasty with intra-arterial milrinone, achieving angiographic improvement in each case. Three patients achieved complete or near-complete neurological recovery, whereas one suffered a DCI-related infarction with a mild residual deficit. Discussion CVS following AVM rupture often occurs later and behaves differently than vasospasm after aSAH, yet it is typically managed with the same protocols due to the lack of specific guidelines. Treating AVM-related vasospasm identically to aSAH vasospasm may be suboptimal given the distinct hemodynamic context. Our cases highlight the value of vigilant neurocritical care monitoring: daily TCD assessments with Lindegaard ratio calculations allowed early identification of sonographic vasospasm and guided timely intervention, potentially averting secondary ischemic injury. However, our experience also shows that standard aSAH vasospasm therapies are not always effective in AVM cases, highlighting the urgent need for research into the unique mechanisms of post-AVM vasospasm and the development of targeted treatments. Conclusion The effectiveness of aSAH-based vasospasm management in ruptured AVMs remains uncertain, but it is the pragmatic standard of care. Dedicated studies and registries are needed to develop evidence-based, AVM-specific vasospasm guidelines. In the meantime, proactive TCD monitoring and individualized interventions should be employed to help prevent DCI and infarction and improve patient outcomes. This abstract is funded by: N/A
Carrizosa et al. (Fri,) studied this question.