Abstract 359: Complex Case of Managing Recurrent Vasospasms and Feverssecondary to Subarachnoid Hemorrhage and Ruptured Left Anterior Communicating Artery Aneurysm in a Patient with uniqueNeuro‐vascular Anatomy

Subarachnoid hemorrhage (SAH) complicated by vasospasm and fever remains a significant therapeutic challenge, particularly in patients with atypical cerebrovascular anatomy. Refractory vasospasm contributes substantially to delayed cerebral ischemia and poor neurologic outcomes, while fever and autonomic instability further worsen prognosis. Existing treatments, including intra‐arterial calcium channel blockers and balloon angioplasty, offer inconsistent and often transient benefit, underscoring the need for adjunctive strategies. We present a 50‐year‐old African American female with uncontrolled hypertension and obesity who presented with sudden severe headache and was found to have SAH from a ruptured anterior communicating artery aneurysm. She underwent emergent craniotomy, intraoperative coiling following aneurysm re‐rupture, and required massive transfusion. Her postoperative course was marked by waxing and waning consciousness, fluctuating fevers, recurrent leukocytosis, and evolving cerebral infarcts. Vasospasm management required multiple angiographic evaluations and intra‐arterial verapamil infusions. Initial control angiograms demonstrated impaired distal left ACA filling, prompting selective left A3 infusion of 5 mg verapamil with transient improvement but recurrent spasm. Balloon angioplasty was deferred given rupture risk. Subsequent angiograms revealed progressive vasospasm involving left ACA A1, MCA M1, and bilateral distal ACA branches, with additional moderate spasm of the supraclinoid ICA and contralateral MCA. Serial intra‐arterial verapamil infusions (5‐15 mg) were administered into the ACA, MCA, and ICA segments, with temporary caliber improvement but frequent recurrence. A solitaire device was deployed for mechanical dilation of the MCA, followed by further superselective verapamil infusions, ultimately improving perfusion though distal ACA occlusion persisted. Concomitant cervical ICA irregularities reflected underlying atherosclerosis and instrumentation‐related spasm, partially responsive to volume expansion and blood pressure management. The patient's course was further complicated by neuro‐storm episodes with tachycardia, hypertension, and febrile spikes. Acetaminophen alone was insufficient to control central fever, which improved following bromocriptine initiation. Blood pressure goals were carefully titrated (160‐180 mmHg) to balance cerebral perfusion against hemorrhagic risk. Additional interventions included tracheostomy, IVC filter for DVT, PEG placement, and prolonged ventilatory support. CT imaging demonstrated diffuse cerebral edema, evolving infarcts, petechial hemorrhage, and left‐to‐right midline shift. This case underscores the complexity of managing recurrent vasospasms and central fever in SAH. Despite aggressive use of intra‐arterial verapamil and supportive measures, vasospasms repeatedly recurred, challenging the role of verapamil as the standard agent. While balloon angioplasty remains a potential alternative, the risk of rupture in the setting of recent aneurysmal hemorrhage limited its use here. The case also illustrates the potential adjunctive role of bromocriptine in refractory central fever, though its mechanism and safety profile in neurocritical care populations remain insufficiently studied. In summary, the patient's atypical vascular anatomy, recurrent neuro‐storms, and hemodynamic instability highlighted the limitations of current protocols. This case emphasizes the need for further investigation into multimodal approaches for SAH‐associated vasospasm, including comparative trials of intra‐arterial vasodilators, endovascular strategies, and pharmacologic adjuncts for autonomic dysregulation. Expanding evidence in these domains is critical to improving morbidity and mortality for patients with aneurysmal SAH.