J Neurocrit Care.  2022 Dec;15(2):141-145. 10.18700/jnc.220059.

Cerebral hyperperfusion syndrome after endovascular stent graft reconstruction for postirradiated carotid blowout syndrome: a case report

• Huang YC
• Lin YH
• Lee CW
• Liao TW

• KMID: 2538773
• DOI: http://doi.org/10.18700/jnc.220059

Abstract

Background
Cerebral hyperperfusion syndrome (CHS) is a failure of autoregulation after a revascularization procedure. It has rarely been reported in patients with no pre-existing cerebral hypoperfusion.
Case Report
We present a rare case of a patient who underwent stent graft implantation to treat postirradiated carotid blowout syndrome. The patient developed hypertension, focal neurological deficit, and seizures after the procedure; neuroimages revealed ipsilateral cerebral edema, swelling, and increased cerebral perfusion. CHS was diagnosed based on clinical and radiological findings. The patient recovered gradually after receiving supportive care.
Conclusion
Owing to the risk of CHS, monitoring for cerebral perfusion and prevention of hypertension is suggested for patients who undergo stent graft placement for postirradiated carotid blowout syndrome.

Keyword

Cerebral hyperperfusion; Carotid blowout; Stent graft; Irradiation

Figure

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  Fig. 1. Left carotid blowout syndrome diagnosed using preoperative computed tomography angiography. (A) Axial computed tomography (CT) revealing irregular focal protrusion of the left common carotid artery (arrow). (B) Sagittal reformatted CT depicting the location of a pseudoaneurysm (arrow) in relation to the surrounding free flap. No obvious stenosis noted in the carotid artery.

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  Fig. 2. Endovascular treatment for carotid blowout syndrome. (A) Lateral view of the left common carotid revealing a pseudoaneurysm of the left distal common carotid artery (black arrow) corresponding to the computed tomography angiography finding. (B, C) After placement of a stent graft (white arrows) and coils (white arrowhead), the pseudoaneurysm was obliterated. The diameter of the carotid artery did not change considerably after the procedure.

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  Fig. 3. Postoperative neuroimaging findings. (A) Non-contrast computed tomography (CT) revealing substantial sulcal effacement at the left frontoparietal lobe, suggestive of cerebral swelling. No frank hypodensity or hemorrhage is observed. (B, C) CT perfusion revealing elevated cerebral blood flow (B) and cerebral blood volume (C) of the left posterior frontal and parietal lobe, and CT angiography revealing dilatation of the left convexity leptomeningeal arteries compared to those in the contralateral right hemisphere. (D, E) Magnetic resonance imaging revealed subcortical hyperintensity on the fluid-attenuated inversion recovery image but not on the diffusion-weighted image, suggestive of vasogenic edema.

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