Introduction: Cerebral Hyperperfusion syndrome (CHS) is a clinical syndrome of hypertension, headache, neurological deficits, with or without seizures, following a revascularization procedure. It is characterized by an excessive and sudden increase in cerebral blood flow. The mechanism is largely not understood but theories involve impaired cerebrovascular autoregulation (thought to be mitigated by collateral circulation), free radical damage, and baroreceptor reflex damage, possible from the procedure itself1 . Common presentations include severe ipsilateral headache to the side of the lesion with typical onset within 12 hours to 6 days, but can occur up to one month, after carotid revascularization processes2 . Investigations include imaging with CT or MRI, or transcranial color duplex to measure velocity in the middle cerebral artery as a correlate of cerebral blood flow3 . The hallmark of management is blood pressure regulation, in order to prevent and limit neurological complications.
Case: The patient is a 71M with PMH HTN not on any antihypertensives, HLD, DM2, OSA on CPAP, Recurrent prostate cancer s/p XRT on Leuprolide, Tobacco use 60 pack years in remission, who was initially admitted with Severe Carotid Artery Stenosis. He underwent R Carotid Artery endarterectomy and subsequent R neck hematoma evacuation on the same day, and was discharged on POD#3 with no noted complications. At home, he developed a severe right sided headache with severely elevated home blood pressure and presented to the nearest emergency room as advised by his physician. On examination, he had right neck swelling with left tracheal deviation. Neurological exam was unremarkable with no focal deficits. CT angiogram revealed a new 5 x 6cm R neck hematoma and patient underwent emergent surgical evacuation. Scheduled beta blockers were initiated postoperatively; however, patient had resulting symptomatic fluctuant blood pressures. Shared decision making with the patient, neurology and neurosurgery resulted in the cessation of the beta blockers. Patient remained in hospital for monitoring for 3 days, with normalization of his blood pressure, and was safely discharged without further complications.
Discussion: This case emphasizes the multifaceted complexity of CHS, emphasizing the need for heightened clinical awareness, patient education and individualized management approaches. Risk factors for CHS, including prolonged duration of severe carotid artery stenosis, hypertension, and older age, are common amongst most patients who undergo carotid artery endarterectomy or stenting2 . Notably, CHS can develop up to one month post-procedure, highlighting the importance of educating patients about diligent home blood pressure monitoring and recognizing red flag symptoms and signs. In this case, the administration of beta-blockers, a common therapeutic approach, led to further complications of symptomatic hypotension, necessitating discontinuation. Collaborative decisionmaking involving multiple medical specialties played a pivotal role in guiding therapeutic interventions and decisions. Continued research into CHS mechanisms and optimal management strategies is ongoing and important in optimizing outcomes. Nevertheless, as demonstrated by this case, the fundamental principles of effective patient communication, ease of access to care, and prompt coordination of management are equally crucial in enhancing patient outcomes.