Abstract Introduction Intra-arterial (IA) milrinone is used as a rescue therapy for refractory cerebral vasospasm. However, paradoxical hemodynamic worsening during continuous IA milrinone infusion has not been reported in the literature. We present a unique case of this phenomenon in a patient with early refractory vasospasm following a ruptured arteriovenous malformation (AVM). Case Description A 37-year-old man with a ruptured right frontal AVM (causing intracerebral and intraventricular hemorrhage) underwent emergency craniotomy with complete AVM resection and placement of a ventricular catheter for intracranial pressure monitoring. In the immediate postoperative period, he developed early severe cerebral vasospasm refractory to standard therapies. Transient improvement was achieved with intra-arterial milrinone boluses, but recurrent vasospasm prompted initiation of a continuous selective IA milrinone infusion via a microcatheter in the right middle cerebral artery (MCA) at 2 μg/kg/min. Shortly after initiating and progressively uptitrating the infusion, the patient experienced acute neurological decline with an ipsilateral drop in regional cerebral oxygen saturation (near-infrared spectroscopy, NIRS) and transcranial Doppler (TCD) evidence of severe vasospasm (right MCA mean flow velocity 423 cm/s; Lindegaard index 9). This sequence suggested a paradoxical vasospasm exacerbation due to the IA milrinone infusion, potentially compounded by local microcatheter-induced arterial irritation. The infusion was promptly discontinued while leaving the microcatheter in place, after which cerebral flow velocities normalized (Lindegaard index decreased to 2.7) and NIRS values recovered. Given the persistent high risk of critical vasospasm, the microcatheter was then removed and definitive rescue therapy was performed via intracranial stent placement, resulting in subsequent clinical stabilization. Discussion This case illustrates an unexpected paradoxical aggravation of vasospasm during IA milrinone therapy, an effect not previously described. We hypothesize two not mutually exclusive mechanisms: (1) focal mechanical stimulation from the microcatheter triggering segmental vasoconstriction, and (2) a pharmacodynamic effect of high-concentration milrinone in a region of impaired autoregulation, leading to distal perfusion imbalance. Immediate re-evaluation using noninvasive monitoring (e.g., detection of ipsilateral NIRS desaturation and markedly elevated TCD velocities with a high Lindegaard index) was crucial to recognize the paradoxical response, halt the infusion, and document subsequent improvement—supporting a causal relationship with the therapy. Given the ongoing risk of cerebral ischemia in refractory vasospasm, endovascular stenting provided stabilization in this patient. As this is a single case, we emphasize the need to individualize intra-arterial vasodilator therapy and maintain vigilant monitoring to identify atypical responses, which can be rapidly reversed with timely intervention. This abstract is funded by: N/A
Carrizosa et al. (2026) studied this question.