Retinal hemorrhage as an initial sign of cerebral hyperperfusion syndrome after carotid artery stenting

Abstract

Dear editor,In patients with carotid artery stenosis, cerebral reperfusionafter carotid artery revascularization, such as carotidendarterectomy (CEA) or carotid artery stenting (CAS),may cause cerebral hyperperfusion syndrome (CHS) [1, 2].If not treated properly, CHS can result in severe brainedema, intracerebral or subarachnoid hemorrhage, and evendeath. Therefore, early detection of CHS is of criticalimportance. We present a rare case of retinal hemorrhage asthe initial sign of CHS after CAS.A 62-year-old man was admitted because of amaurosisfugax involving his left eye and temporary right hemi-paresis. There was no high-signal intensity on the diffusion-weighted image (DWI). Trans-femoral cerebral angiogra-phy (TFCA) revealed severe stenosis (approximately 90%)of the left proximal internal carotid artery (Fig. 1a). Weconcluded that this was a symptomatic lesion so that CASwas performed under distal embolic protection without anycomplications (Fig. 1b). We did not evaluate cerebral bloodflow (CBF) measurement for this patient before performingCAS.The blood pressure (BP) of the patient was about 160/100 mmHg before the procedure and decreased to about120/80 mmHg in the post-stenting period. On the morningon the 3rd postoperative day, the patient complained ofblurred vision in his left eye with a left temporo-parietalheadache, and he became lethargic. Suspecting an intrace-rebral hemorrhage by CHS, a brain computed tomographywas obtained, which showed no specific findings. On theDWI, there was no evidence suggesting an acute infarction;however, the perfusion-weighted image showed shorteningof the mean transit time (MTT) and increased cerebralblood volume (CBV) in the left fronto-parietal area(Fig. 1c). Immediate reduction of the systemic arterialblood pressure was achieved with intravenous labetalol. Onthe next day, an ophthalmologic examination was per-formed. Retinal hemorrhage in the left lower quadrant ofthe macula was observed, which was the likely cause of theblurred vision (Fig. 1d). CHS was confirmed based onclinical symptoms, radiographic findings, and the results ofan ophthalmologic examination. On the 7th postoperativeday, a follow-up TFCA was performed, which showed theleft ophthalmic artery to be increased in size and densitycompared to the pre-stenting TFCA (Fig. 1e), suggestingthat the increased blood flow to the left ophthalmic arterymight cause retinal hemorrhage.The general clinical features of CHS include the triad ofipsilateral headaches, seizures, and neurologic impairment(ataxia, visual disturbance, focal limb weakness) unrelatedto thromboembolism, and without evidence of new infarc-tion. In this case, CHS was confirmed by clinical symptoms(ipsilateral headaches and visual disturbance) and radio-graphic findings (shortening of the MTT, increased CBV,and left ophthalmic artery increased in density and size).Retinal hemorrhage can be caused by chronic hypertension,retinal vein occlusion, retinal artery embolus, diabeticretinopathy, or trauma. The patient had a 10-year historyof hypertension and diabetes, which carries the possibilityof inducing retinal hemorrhage coincidentally. This possi-bility evoked doubt whether or not the retinal hemorrhage