To date, carotid endarterectomy remains the preferred treatment option for carotid stenosis, and its postoperative complications are increasingly studied. It has been clinically found that some patients may develop a state of ipsilateral cerebral tissue hyperperfusion due to postoperative carotid artery opening and increased blood flow. Although most patients have mild symptoms and signs, the condition may progress rapidly or even threaten the patient’s life if adequate attention and timely treatment are not given. 1. Pathophysiological basis (1) Impaired cerebrovascular autoregulation mechanism Patients with severe carotid artery stenosis have impaired cerebrovascular autoregulation mechanism due to the long-term hypoperfusion state of one cerebral hemisphere, and the small intracerebral arteries can be extremely dilated. In CEA, when the internal carotid artery is opened, the blood flow of the internal carotid artery on the operated side increases a lot, but due to the impaired cerebrovascular autoregulation mechanism, the small intracerebral vessels cannot contract and regulate accordingly, which makes the blood flow rate of the ipsilateral intracranial artery increase continuously and the brain tissue of one cerebral hemisphere is overperfused, and the dilated small vessel bed leaks a lot of plasma components, forming vasogenic cerebral edema and leading to the increase of intracranial pressure. Patients clinically present with severe headache and persistently elevated blood pressure. The hypertensive state in turn aggravates the hyperperfusion state of brain tissue, forming a vicious circle. (2) Impaired pressure receptor reflexes The pressure receptors in the carotid arteries are capable of buffering drastic changes in blood pressure; CEA may lead to denervation of the pressure receptors, making the body unable to respond effectively to excessive blood pressure elevation, resulting in increased cerebral perfusion. (3) Trigeminal ganglion vascular reflex Macfarlane et al. proposed an axonal-like trigeminal vascular reflex associated with the pathological life of CHS, suggesting that the failure of self-regulation is due to pathological release of vasoactive neuropeptides, like calcitonin-related peptide or substance P, from nerve fibers in the outer membrane of cerebral vessels in areas of cerebral ischemia, leading to vasodilation and increased blood flow. These nerve fibers originate in the trigeminal ganglion, and removal of the trigeminal ganglion inhibits the increase in cerebral blood flow. These three mechanisms of action lead to an excessive increase in cerebral blood flow, causing cerebral white matter edema. Autopsy results show that the pathological findings of CHS are similar to those of malignant hypertension, including endothelial cell swelling and hyperplasia, erythrocyte extravasation and fibrin-like necrosis. Many studies have shown that CHS is less likely to occur after CEA than CAS. Ogasawara et al. suggested that the peak of CHS is on day 6 after CEA and up to 12 h after CAS, and described some differences between CHS after CAS and CEA: (1) CAS is more likely to have embolic events leading to postoperative ischemic brain injury. (2) The stimulation of carotid pressure receptors during balloon dilation and stent support is greater in CAS, causing a slower heart rate and lower blood pressure for a longer period of time than clamping in CEA. Postoperative rebound hypertension may lead to an increased incidence of cerebral hyperperfusion. (3) Many high-risk patients with CAS are surgical high-risk patients, mostly combined with high-risk factors for CHS, and are more likely to develop hyperperfusion after surgery. 3. Treatment Identification of high-risk patients, early detection of symptoms and symptomatic treatment, and close monitoring of hemodynamics, including control of systolic blood pressure and monitoring of postoperative CBF changes using TCD, are fundamental to treatment. Intraoperative use of a diversion tube should minimize the duration of cerebral ischemia, and strict postoperative blood pressure control can significantly reduce the occurrence of CHS. For severe lesions bilaterally, the use of a small-diameter diverter tube is recommended to reduce the occurrence of postoperative overperfusion. Once the diagnosis is confirmed, antihypertensive, treatment of cerebral edema and anticonvulsant therapy are the basis of treatment. Of these, antihypertensive therapy is key. Because blood flow in CHS patients is pressure-dependent, controlling the drop in blood pressure can lead to rapid relief of symptoms, and even in patients with normal blood pressure, lowering blood pressure can still make symptoms disappear. Most authors recommend that postoperative blood pressure should be reduced to normal or slightly lower levels, and the ideal target blood pressure should be below the threshold that can breach cerebrovascular self-regulation without causing cerebral underperfusion. Strict antihypertensive therapy must be continued until cerebral self-regulation is restored, with bilateral hemispheric homogenization observed according to TCD. There is no definitive evidence as to which particular antihypertensive drug is most effective. It has been suggested that cerebral vasodilators such as dihydropyridazine, nitrates, or calcium antagonists, despite reducing systolic blood pressure, exacerbate cerebral edema and should be avoided. Angiotensin-converting enzyme inhibitors have a limited effect, while angiotensin receptor antagonists have a long half-life and cannot be administered intravenously. β-receptor antagonists reduce arterial pressure within the range of autoregulation and have little effect on intracranial pressure, and can be used to treat hypertensive patients with brain injury, but should be contraindicated in patients with postoperative bradycardia. Labetalol, which has both alpha and beta receptor antagonism, does not directly affect intracranial blood flow, but reduces cerebral perfusion pressure and mean arterial pressure by approximately 30%, and is widely used in CHS. Because post-operative hypertension after CEA is accompanied by increased intracranial and plasma catecholamine concentrations, treatment needs to include centrally acting sympathetic blockers. lower arterial blood pressure, heart rate and cardiac output, resulting in lower cerebral blood flow. In conclusion, labetalol and colistin are the best drugs to treat CHS hyperperfusion, and other vasodilators may exacerbate CHS symptoms. There is no evidence that prophylactic antiepileptic drugs are required before carotid surgery, but if subclinical epileptiform discharges are found on EEG, it is an indication for antiepileptic treatment. a study by Ogasawara et al. showed that preoperative use of the free radical scavenger edaravone effectively reduced the occurrence of hyperperfusion after CEA. 4. Prognosis The prognosis of CHS depends on timely diagnosis and treatment. Although most patients recover completely, those with severe CHS have a poor prognosis. Studies have shown that 30% of patients with severe CHS develop functional impairment, and once cerebral hemorrhage occurs, the mortality rate reaches 50%. In conclusion, CHS is a rare but serious complication after CEA, which directly affects the prognosis of patients. With the widespread implementation of CEA, CHS will become an important factor affecting survival prognosis and should be taken seriously by the majority of clinicians.