Hrev_master Abstract Prevention of disability from cerebrovascular accident through carotid endarterectomy, neurovascular stenting, and endovascular treatment of stroke are among the most promising treatments for neurovascular diseases. Cerebral hyperperfusion syndrome is a rare complication of these procedures, and this case report illus- trates a patient with this condition after carotid endarterectomy. The mechanism of hyperperfusion is thought to be from chronic compensatory small vessel dilation to maintain cerebral perfusion in the context of vascular stenosis. Treatment is largely supportive with strict blood pressure control. As treatment options for neu- rovascular reperfusion become mainstay, emergency clinicians need to be appraised to post procedural complications such as cere- bral hyperperfusion. Introduction Prevention of disability from cerebrovascular accident through carotid endarterectomy, neurovascular stenting, and endovascular treatment of stroke are among the most promising treatments for neurovascular diseases. The rapid increase in these treatment modalities will undoubtedly be accompanied by postprocedural complications.1,2 This case presents the uncommon complication of cerebral hyperperfusion syndrome after a carotid endarterectomy. Case Report The patient is a 70-year-old female with a past medical history of coronary artery disease and carotid stenosis presenting with left- sided weakness, left-sided facial droop, and right gaze deviation. She was 6-days days postoperative from a right carotid endarterec- tomy. She was last seen well when she went to sleep that evening. Her family denied any trauma or concerns during the prior day. Her carotid endarterectomy was reportedly uncomplicated, with her only postoperative problems being elevated blood pressure, managed with oral medication dose adjustments, and feelings of right eye pressure. Her initial vital signs showed a blood pressure of 137/86 mmHg, heart rate of 78 beats per minute, temperature of 36.1 degrees Celsius, respiratory rate of 17 breaths per minute, oxygen saturation of 100% on room air, and blood sugar of 118 mg/dL. Due to her initial physical exam showing left-sided weakness and left facial droop, the initial concern was an acute ischemic stroke, and computed tomography imaging was prioritized. Her blood sugar was 90 mg/dL. While in the computed tomography scanner, the patient had a generalized tonic-clonic seizure, which self- resolved within one minute. The patient’s computed tomography of the brain without con- trast showed asymmetric, ill-defined hypodensities in the right frontal lobe periventricular white matter without intracranial hem- orrhage (Figure 1). Computed tomography angiography did not show cerebrovascular stenosis or occlusion, and perfusion imaging showed symmetric flow and volume throughout the brain. These findings were discussed with the neurointerventional specialist and neurologist and determined to be secondary to cerebral hyperper- fusion syndrome. The patient was admitted to the intensive care unit for strict systolic blood pressure control with a goal of less than 130 mmHg. This was achieved with intermittent intravenous Emergency Care Journal 2025; volume 21:14255 [Emergency Care Journal 2025; 21:14255] [page 57] Cerebral hyperperfusion syndrome after carotid endarterectomy: case report David Fine,1,2 John Teijido,1,2 Laurie Benson,1,2 Matthew Treat1,2 1Emergency Medicine Specialists, S. C., Wauwatosa, WI; 2Ascension, St. Louis, MO, United States Correspondence: John Teijido, MD; Emergency Medicine Specialists, S.C., 10625 West North Avenue, Suite 102, 53226 Wauwatosa, WI, USA. Tel.: 414.877.5350 - Fax: 414.877.5360 E-mail: john.teijido@gmail.com Key words: cerebral hyperperfusion syndrome; carotid endarterecto- my; carotid stenting. Conflicts of interest: all authors have no conflicts of interest to dis- close. Contributions: DF, JT, conception and design of work, analysis and data interpretation, drafting work, substantial critical review, final approval, and agreement to being fully accountable for all aspects of work; LB, conception and design of work, substantial critical review, final approval, and agreement to being fully accountable for all aspects of work; MT, drafting work, substantial critical review, final approval, and agreement to being fully accountable for all aspects of work. Ethics approval: not applicable Informed consent: informed consent was obtained from the patient in this study. Availability of data and materials: all data generated or analyzed during the study are included in this published article. . Received: 16 August 2025 Accepted: 2 October 2025. Early view: 15 October 2025. This work is licensed under a Creative Commons Attribution 4.0 License (by-nc 4.0). ©Copyright: the Author(s), 2025 Licensee PAGEPress, Italy Emergency Care Journal 2025; 21:14255 doi:10.4081/ecj.2025.14255 Publisher's note: all claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. labetalol 10 to 20mg. Intravenous levetiracetam 1000mg followed by 500mg twice daily was given for seizure prophylaxis and the patient made gradual improvements in speech and strength. She was transferred to a rehabilitation facility and later she was dis- charged home with only minimal left leg weakness as her only neurologic deficit. Discussion Cerebral Hyperperfusion Syndrome (CHS) is a rare complica- tion of Carotid Endarterectomy (CEA), Carotid Angioplasty with Stenting (CAS), and endovascular thrombectomy.1,2 The proposed mechanism of hyperperfusion is related to the chronic compen- satory small vessel dilation to maintain cerebral perfusion in the context of vascular stenosis. Autoregulation is initially impaired in these vessels when the stenosis is repaired. Endothelial dysfunc- tion due to free radicals and the resulting hyperperfusion damages the capillary beds leading to cerebral edema and hemorrhage.2-4 Presenting symptoms occur within two weeks of CEA including ipsilateral positional headaches, ipsilateral eye or facial pain, seizures, and intracerebral hemorrhage.2 Risk factors include revascularization of high-grade (greater than 80 percent) stenosis, recent cerebral infarction, contralateral carotid occlusion, and post-operative hypertension.5 CHS after CEA occurs at rates of 1 to 3 percent. Associated intracerebral hemorrhages in this cohort have an incidence of 0.6 percent with mortality as high as 26 percent.3,4,6 CHS is primarily a clinical diagnosis. Identifying cerebral edema or intracranial hemorrhage associated with it is achieved with Computed Tomography (CT), Computed Tomography Angiography (CTA), or Magnetic Resonance Imaging (MRI) with T2 or FLAIR sequences. Imaging findings are ipsilateral to the side of the carotid artery procedure. Edema is classically within the white matter although the cortex may also be involved. These modalities can assist in ruling out alternative pathologies including vessel dissection or rupture. Diffusion weighted imaging on MRI distinguishes cerebral ischemia from edema. CT perfusion may see increased cerebral blood flow, increased cerebral blood volume, shortened mean transit time, and shortened time to peak. Flow alterations may also be identified on Near-Infrared Spectroscopy (NIRS) or transcranial doppler.2,3,5,7-9 Evaluations with these modalities have shown cerebral artery flow velocity up to three times the contralateral hemisphere; however, the degree of increase does not correlate with disease severity. Even moderate hyperperfusion (20 to 44 percent increase) may still cause cerebral hyperperfusion syndrome.6 Prevention with strict post-operative hypertensive control is recommended with systolic blood pressure goals <140/90 mmHg or within 20% of baseline blood pressure in the context of pre- existing hypertension. Recommended medications include labetalol, clonidine, nitroglycerin, and, particularly, nicardipine, as it is rapidly titratable.2,6 Conclusions Cerebral hyperperfusion syndrome is an uncommon complica- tion of cervical or cerebrovascular reperfusion. As treatment options for neurovascular reperfusion continue to expand, vigi- lance of post procedural complications such as this will be critical to help prevent further disability. Case Report [page 58] [Emergency Care Journal 2025; 21:14255] Figure 1. Axial view (a) and coronal view (b) of computed tomography of the brain showing right frontal hypodensities as indicated by the blue arrows. References 1. Galyfos G, Sianou A, Filis K. Cerebral hyperperfusion syn- drome and intracranial hemorrhage after carotid endarterecto- my or carotid stenting: A meta-analysis. J Neurol Sci 2017;381:74-82. 2. Lin YH, Liu HM. Update on cerebral hyper-perfusion syn- drome. J Neurointerv Surg 2020;12:788-93. 3. Diana F, Frauenfelder G, Botto A, Saponiero R, Romano DG. Cerebral hyperperfusion syndrome after intracranial stenting: Case report and systematic review. Interv Neuroradiol 2021;27:843-9. 4. Van Mook WN, Rennenberg RJ, Schurink GW, et al. Cerebral hyperperfusion syndrome. Lancet Neurol 2005;4:877-88. 5. Ortigosa Arrabal MP, Delgado Gil V, de la Cruz Cosme C. Cerebral hyperperfusion syndrome in the emergency depart- ment. Emergencias 2022;34:404-6. English, Spanish. 6. Jeffrey J. Complications of Carotid Endarterectomy. In: UpToDate, Connor RF (Ed), Wolters Kluwer. 7. Karapanayiotides T, Meuli R, Devuyst G, et al. Postcarotid endarterectomy hyperperfusion or reperfusion syndrome. Stroke 2005;36:21-6. 8. Moulakakis KG, Mylonas SN, Sfyroeras GS, Andrikopoulos V. Hyperperfusion syndrome after carotid revascularization. J Vascular Surg 2009;49:1060-8. 9. Wang D, Zhu F, Fung KM, et al. Predicting cerebral hyperper- fusion syndrome following superficial temporal artery to mid- dle cerebral artery bypass based on intraoperative perfusion- weighted magnetic resonance imaging. Sci Rep 2015;5:14140. Case Report [Emergency Care Journal 2025; 21:14255] [page 59]