Hyperperfusion syndrome (CHS) is a rare but severe complication that occurs after carotid endarterectomy (CEA). It was first reported by Sundt et al. in 1981. It mainly manifested as sudden headache and neurological function after surgery. Defects, seizures, and intracranial hemorrhage. Meyers first proposed in 1984 that the possible mechanism of hyperperfusion syndrome is the disorder of cerebral blood flow autoregulation (CA).
With the development of neurological intervention techniques, hyperperfusion syndrome of the brain can also be seen after carotid artery stenting (CAS) or intracranial arterial stenting. In 2001, Liu et al. reported the first case of middle cerebral artery (MCA) stenting. Hyperperfusion syndrome in patients. Since then, with the popularity of endovascular stent angioplasty, brain hyperperfusion syndrome has received more and more attention. The most serious type of cerebral hyperperfusion syndrome is intracranial hemorrhage. The literature reports that the incidence of hyperperfusion syndrome after carotid endarterectomy is 3.4%, and the incidence of intracranial hemorrhage is about 0.1%; the brain after carotid stenting The incidence of hyperperfusion syndrome is about 2.2%, and the incidence of intracranial hemorrhage is about 0.8%. Although the incidence of intracerebral hemorrhage caused by cerebral hyperperfusion syndrome is low, the mortality and the rate of severe disability are extremely high. This is one of the most dangerous complications after neurointervention. This article briefly reviewed the progress of brain perfusion syndrome. Overview.
1. Clinical characteristics
1.1 Clinical manifestations
The clinical symptoms of hyperperfusion syndrome are caused by intracranial hemorrhage caused by hyperperfusion or vasogenic brain edema, mainly after carotid endarterectomy, after carotid stenting, or after intracranial arterial stenting. Headache, cognitive impairment, disturbance of consciousness, seizures, and treatment of neurological deficits, as well as symptoms of increased intracranial pressure such as nausea, vomiting, and elevated blood pressure. Sometimes it is similar to stent thrombosis, embolization of atherosclerotic plaque, or transient ischemic attack (TIA), and differential diagnosis should be noted. About 59% of patients with hyperperfusion syndrome can develop headaches, which often occur on the surgical side, and are usually moderate to severe pulsatile headaches like migraines.
In addition, the symptoms of neurological deficits caused by hyperperfusion syndrome of the brain are mainly manifested as decreased vision, aphasia or decreased muscle strength. The neurological deficits of simple cerebral engorgement hyperperfusion syndrome are often transient, and there is no new imaging infarcts. . Seizures are usually partial seizures and progressively progress to a full tonic-clonic seizure (GTCS), which can also be characterized as a sudden full-blown seizure, and can persist for up to 2 weeks after surgery. One-third of brain over-perfusion complexes Symptoms were manifested as epileptic seizures, 1/3 only showed partial paralysis, and more than 1/3 showed seizures and hemiplegia. Studies have shown that carotid artery stenting is different from carotid endarterectomy for cerebral hyperperfusion syndrome. The former occurs within hours after surgery, and the latter occurs within 3 to 6 days after surgery. Occurred 28 days after surgery.
PET, SPECT, transcranial Doppler (TCD), CT and MRI can be used for the diagnosis of hyperperfusion syndrome. SPECT and TCD are currently the most commonly used clinical methods, followed by CT and MRI. Different examination methods have different focuses. CT is a quick and effective auxiliary diagnosis method. It can not only identify whether there is an intracranial hematoma, but also differentiate it from transient ischemic attack and acute ischemic stroke. Transient ischemic attack and acute ischemic stroke usually have no abnormal changes on CT, and CT may show swelling of the brain tissue, brain sulcus, and gyrus disappearance after the onset of cerebral hyperperfusion syndrome. These are all excessive brain Indirect signs of perfusion syndrome.
Diffusion-weighted imaging (DWI) can be used to exclude acute ischemic stroke, and T2WI and FLAIR imaging can better show cerebral edema. SPECT can show early signs of brain hyperperfusion syndrome not found in CT. TCD has many advantages in the diagnosis and treatment of hyperperfusion syndrome of the brain. It is a non-invasive method that can be repeatedly operated. It can directly and real-time monitor cerebral blood flow (CBF) and cerebral blood flow velocity, and can be preoperative blood. Flow status was used as a reference baseline and compared with postoperative patients to prevent the occurrence of hyperperfusion syndrome.
At present, it is believed that the cerebral blood flow velocity after surgery is more than 100% higher than before surgery, suggesting cerebral hyperperfusion syndrome. CT perfusion imaging (CTP) is also helpful in the diagnosis of cerebral hyperperfusion syndrome. Tseng et al. Comparative observation of preoperative and postoperative CTP images in 55 patients with carotid stent angioplasty and found mean transit time (MTT) and hyperperfusion syndrome The occurrence is obviously related. The prolongation of the mean transit time was positively correlated with the degree of intracranial vascular stenosis and the decrease of cerebral blood flow. Decreased cerebral blood flow, prolongation of mean transit time, and slight increase in cerebral blood volume (CBV) prompted intracranial vasodilation and cerebral blood flow was automatically Regulatory mechanisms are impaired and there is an increased risk of postoperative hyperperfusion syndrome.
The Arterial Spin Labeling (ASL) is similar to CTP but does not require additional contrast media for brain tissue perfusion examination in patients with renal failure. PET can also provide valuable information for the diagnosis of hyperperfusion syndrome of the brain. Matsubara et al. compared PET imaging before and after carotid stent angioplasty and found that cerebral blood flow, cerebral perfusion pressure (CPP), and cerebral oxygen metabolism were rapid. Increase and peak, and only a small increase in cerebral blood flow reserve capacity may be one of the mechanisms of brain hyperperfusion syndrome. Functional near-infrared spectroscopy imaging (fNIRS) is a new, non-invasive method for continuous monitoring of oxygenation index in brain tissue in real time. It can effectively predict the occurrence of hyperperfusion syndrome in the brain.
2. Risk factors
It has been reported in the literature that risk factors for hyperperfusion syndrome include women, advanced age (>75 years), hypertension, diabetes, recent stroke history, severe carotid stenosis (>90%) and severe stenosis of the contralateral carotid artery (> 80%) or occlusion. Recent studies have shown that certain imaging changes are also risk factors for cerebral hyperperfusion syndrome. For example, acetazolamide detects cerebrovascular reactivity, and patients with cerebrovascular reactivity less than 20% have a higher risk of hyperperfusion syndrome The CTP showed that the preoperative ipsilateral cerebral blood flow was less than 80% of the contralateral side, and the mean transit time was higher than 3 seconds was also a risk factor for postoperative cerebral hyperperfusion syndrome. The integrity of the Willis ring is a protective factor for hyperperfusion syndrome.
Katano et al.'s study showed that patients with severe carotid artery stenosis developing in the contralateral anterior communicating artery (ACoA) and the anterior segment of the anterior cerebral artery (ACA) have a lower risk of postoperative cerebral hyperperfusion syndrome. The mechanism may be the carotid artery. Sudden increase in cerebral blood flow after stenting was performed by diverting the anterior communicating artery and the contralateral anterior cerebral artery A1 segment to the contralateral middle cerebral artery. Recent stroke history can significantly increase the risk of cerebral hyperperfusion syndrome after carotid stenting. Xu et al. performed a retrospective analysis of the cerebral hyperperfusion syndrome that occurred after intracranial arterial stenting and found that the risk of cerebral hyperperfusion syndrome was higher in patients who underwent intracranial arterial stenting within 3 weeks of stroke.
3. Mechanism of occurrence
At present, the mechanism of brain hyperperfusion syndrome has not yet been fully elucidated, and it is considered to be the result of a combination of mechanisms.
3.1 Cerebral blood flow autoregulation disorder
The normal brain has the ability to automatically regulate cerebral blood flow and maintain normal intracranial pressure by altering cerebral blood flow. In 1968, Waltz first discovered the damage of cerebral blood flow to the autoregulation of cerebral blood flow. Through the preparation of cat middle cerebral artery occlusion (MCAO) model, it was found that with the increase of blood pressure, cerebral blood flow in ischemic brain tissue fluctuates significantly. Cerebral blood flow in non-ischemic brain tissue remains unchanged, suggesting that cerebral ischemia may impair the ability of autoregulation of cerebral blood flow. The mechanism may be severe stenosis of the supplying artery leading to insufficient perfusion of the distal brain tissue, chronic expansion of the blood vessel, loss of self-regulation, When the cerebral blood flow suddenly increases, the vasoconstriction is difficult and the capillary bed cannot be protected, resulting in intracranial hemorrhage.
3.2 Microvascular disease
Patients with severe internal carotid artery stenosis are associated with hypertension. Preoperative long-term hypertension can lead to dysfunction of vascular endothelial cells and microvascular disease, thereby destroying the blood-brain barrier (BBB). Animal experiments showed that blood-brain barrier disruption exists in animal models of hyperperfusion brain syndrome.
3.3 The role of nitric oxide and free radicals
Nitric oxide can dilate blood vessels, increase cerebrovascular wall permeability, thus impaired autoregulation of cerebral blood flow, disruption of blood-brain barrier, and induce hyperperfusion syndrome. Dohare et al. prepared an animal model of middle cerebral artery ischemia-reperfusion injury and found that a large amount of nitric oxide produced by nitric oxide synthase (NOS) participates in nerve injury, causing rupture of lipid membranes and destruction of blood-brain barrier, resulting in excessive brain The incidence of perfusion syndrome.
4. Postoperative blood pressure increase Baroreceptor dysfunction can lead to persistently elevated blood pressure and increase the risk of hyperperfusion syndrome. Recent studies have shown that the carotid stenting process stimulates carotid arterial baroreceptors during balloon angioplasty, leading to a transient decrease in heart rate, a decrease in blood pressure, and subsequent blood pressure rebound that may induce hyperperfusion syndrome. In addition, elevated norepinephrine levels, increased release of vasoactive peptides, the use of anesthetics, and perioperative psychological stress can lead to increased postoperative blood pressure, thereby increasing the risk of hyperperfusion syndrome.
4. Diagnostic criteria
The diagnosis of hyperperfusion syndrome is mainly based on the symptoms of headache, seizures and focal neurological deficits after revascularization. It should be noted that it is distinguished from transient ischemic attack and ischemic stroke, especially seizures. Impaired consciousness is more likely to diagnose brain hyperperfusion syndrome. If the above-mentioned clinical symptoms occur, and CTP, TCD, and other auxiliary examinations confirm the presence of excessive brain tissue perfusion, hyperperfusion syndrome may be considered.
5.1 Complete Auxiliary Inspection
Preoperative digital subtraction angiography (DSA) can accurately determine the development of the Willis ring and collateral compensation. CTP and TCD can help to understand the baseline level of cerebral blood flow, average blood flow velocity and other parameters. Preoperative and postoperative contrasts can accurately predict the occurrence of hyperperfusion syndrome. MRI, especially DWI, can accurately indicate whether there is an acute phase infarction and exclude the history of recent stroke.
5.2 Control Blood Pressure
Strict control of blood pressure is currently the most clinically important method to prevent hyperperfusion syndrome. Some patients have a higher risk of cerebral hyperperfusion syndrome even with normal blood pressure. Blood pressure control should continue until cerebrovascular reactivity returns to normal. TCD helps to understand cerebrovascular reactivity. There is currently no drug that directly reduces cerebral blood flow. Some vasoconstrictor drugs may be beneficial for the prevention of hyperperfusion syndrome, and sodium nitroprusside and calcium antagonists may increase cerebral blood flow and should be avoided in clinical applications. Studies have shown that although alpha-adrenergic receptor blockers and beta-adrenergic receptor blockers, labetalol, do not directly reduce cerebral blood flow, they can prevent brain by reducing mean arterial pressure and cerebral perfusion pressure. Hyperperfusion syndrome.
5.3 Oxygen radical scavenger
Oxygen free radicals are one of the mechanisms of brain hyperperfusion syndrome. Oxygen radical scavengers such as edaravone can prevent the occurrence of hyperperfusion syndrome after carotid endarterectomy and also prevent carotid stent angioplasty. It also provides new ideas for the occurrence of cerebral hyperperfusion syndrome after intracranial arterial stenting.
5.4 surgical methods and time
In 2009, Yoshimura et al used staged carotid artery angioplasty to treat patients with severe carotid artery stenosis at high risk of hyperperfusion syndrome. The first treatment was to select a small balloon (3 mm in diameter) for dilatation. After SPECT imaging showed relief of high perfusion signs, In the second-stage stenting, 9 cases of patients with staged treatment had no case of cerebral hyperperfusion syndrome, while 9 cases of primary stenting had cerebral hyperperfusion syndrome in 5 cases and epileptic state in 1 case ( SE). Mo et al. conducted a retrospective analysis of 44 high-risk patients with hyperperfusion syndrome, and found that staging treatment could reduce the risk of hyperperfusion syndrome in the brain, which needs to be confirmed by large-scale randomized controlled trials. Correct operative time is also one of the important measures to reduce hyperperfusion syndrome.
Studies have shown that patients with carotid artery stenosis undergoing carotid artery stenting within 1 week after stroke have a higher risk of postoperative cerebral hyperperfusion syndrome. Xu et al. Screened risk factors for cerebral hyperperfusion syndrome after intracranial arterial stenting and found that intracranial arterial stenting was a risk factor for hyperperfusion syndrome in the brain within 3 weeks after stroke.
5.5 Choice of anesthetic
Although most carotid stent angioplasty uses local anesthesia, intracranial arterial stent angioplasty generally uses general anesthesia. Some volatile halogenated hydrocarbon anesthetics such as isoflurane have a vasodilatory effect and are suitable for patients with traumatic brain injury. However, high doses of isoflurane can affect the autoregulation of cerebral blood flow and may increase the risk of cerebral hyperperfusion syndrome.
At present, there is no effective treatment method recommended by the guideline for hyperperfusion syndrome, the main clinical prevention. Once it happens, it should be handled urgently. For brain edema, mannitol and hypertonic saline can be used to reduce intracranial pressure, but its potential effects and long-term prognosis are still unclear. Other drugs, such as hormones and barbiturates, may also be effective in some patients with cerebral edema. Prophylactic use of antiepileptic drugs (AEDs) is not recommended, but antiepileptic drugs can be used if the electroencephalogram shows unilateral periodic discharges (LPDs) or clinical epileptic seizures. For patients with intracerebral hemorrhage, whether or not to remove the hematoma by surgery should be determined according to the site and degree of bleeding.
Brain hyperperfusion syndrome is a very dangerous post-neural complication. Although the incidence is low, the mortality is extremely high. The prevention of hyperperfusion syndrome of the brain mainly depends on strict control of blood pressure, improvement of perioperative imaging examinations, and development of reasonable surgical strategies and timing. Accurate judgment of cerebral blood flow autoregulation and cerebral blood flow reserve is the key to prevent postoperative cerebral hyperperfusion syndrome. However, there is no large-scale clinical trial for cerebrovascular reactivity and cerebral blood flow reserve. The development of imaging technology and the rise of more non-invasive methods may provide more accurate prevention and treatment strategies for hyperperfusion syndrome.