Carotid Endarterectomy (CEA) and medical therapy reduces the risk of recurrent stroke for individuals with symptomatic carotid artery disease (CAD) with ≥50% arterial stenosis. Reversible Cerebral Vasoconstriction Syndrome (RCVS) is a rare complication of CEA.

A 75-year-old female with a history of atrial fibrillation and depression on fluoxetine underwent CEA and innominate artery stenting for asymptomatic high-grade CAD. Three days after carotid revascularization, she developed recurrent thunderclap headaches characterized as severe, holocephalic, apoplectic in onset, and lasting several minutes. 

Over the next eleven days, she reported recurrence of these headaches, prompting evaluation at a local hospital. She was found to have elevated blood pressures, and initial CT imaging of the head demonstrated unilateral acute subarachnoid hemorrhage overlying the right cerebral hemisphere. CT angiogram of the head demonstrated moderate right M2 segment middle cerebral artery calcification with moderate-severe stenosis, without other vascular pathology. The presence of subarachnoid hemorrhage prompted transfer to our institution for evaluation and management. MRI Brain did not reveal parenchymal infarction, cerebral microhemorrhage, or other structural pathology. Digital subtraction angiography demonstrated multifocal distal alternating high-grade arterial stenosis, predominantly involving the arterial vasculature supplying the right cerebral hemisphere, sparing the intracranial internal carotid artery, and did not demonstrate intracranial aneurysm. Her RCVS2 score was 10 ^1. Her headache resolved with conservative management while monitored in the hospital. She did not develop focal neurological symptoms and she was eventually discharged with a plan for repeat brain structural imaging. Fluoxetine was discontinued.    

Non-aneurysmal subarachnoid hemorrhage, recurrent thunderclap headache, and multifocal intracranial arterial stenosis should prompt consideration of RCVS among individuals undergoing carotid revascularization.  Impaired autoregulation has been implicated in the development of RCVS following carotid revascularization ^2. Therapeutic anticoagulation and fluoxetine exposure may have also contributed to this patient’s risk of SAH and RCVS