过度灌注综合征

Pathophysiology: Free Radicals
• Unavoided ischemic and ischaemia-reperfusion events during CRV will cause oxygen-derived free radicals,and a free-radical scavenger,that is edaravone, may help to prevent hyperperfusion.
Assistant Examination: CT, MRI, Neck ultrasound, EEG
• CT or MRI can shows either intracerebral oedema or haemorrhage. EEG can demonstrate epileptiform discharge. • The most important purose for CT/MRI is differential diagnosis.,as ischemic stroke can also cause the above symptom. Besides acute carotid thrombopoiesis can also cause ischemic injury, carotid ultrosound should also be applied.
Pathophysiology:Hypertension and Baroreceptor dysfunction
1. Hypertension( occurs 11% after CEA and 13% after CAS in an RCT) can significently increases CBF in impaired autoregulation. And Preoperative hypertension is the single most important determinant of development of postoperative hypertension. 2. Baroreceptor dysfunction can cause a progressive increase BP post-operatively, especially in those with contralateral stenosis. So poor collateral flow and recent (3 months) contralateral CEA are also proved to be related with CHS.
Hyperperfusion Syndrome After Carotid Revasculation (CRV)
Author:Jiao LQ
Introduction
• The two most common interventions used for carotid stenosis are carotid endarterectomy (CEA) and carotid artery stenting (CAS). • Cerebral hyperfusion syndrome (CHS) is characterised by throbbing headache, seizures with frequent secondary generalisation, focal neurological deficits, and intracerebral or subarachnoid haemorrhage. • This sydrome is underestimated in domestic, as an review of Chinese documents from 1978 to 2011 see only 100 CHS cases were reported.
In concusion, with the remove of plaque and under the effect of HBP, a large sum of blood flow over into the brain, and breakthrough of the impaired cerebral autoregulation will happen. This will damage BBB and cause blood components exudation. Direct exposure to blood components may cause epileptiform discharge and focoal neurological deficits.
Pathology
• Descriptions for the pathology come from autopsy of those patients died of ICH induced by CHS. • Autopsy revealed changes resembled the changes seen in malignant hypertension. These changes included hypercellularity and edema of arterial and arteriolar walls. with necrosis, extravasation of erythrocytes. and exudation of fibrin
Definition:Cerebral Hyperperfusion and Cerebral Hyperfusion Syndrome
1.Although cerebral blood flow and perfusion increase in almost all patients following CRV, hyperperfusion is usually defined as a 100% increase in CBF compared to the pre-operative baseline. 2. CHS is a series of “syndromes” containing headache, seizures and focal neurological deficits. 3. Hyperperfusion is seen in most cases of CHS, but symptoms can also occur in patients with only moderate increases in CBF. However, the risk of developing CHS is 10 times higher in patients with hyperperfusion than in those without. In one study, ICH developed in 3.3% of patients with hyperperfusion vs. only 0.24% of those without.
CΒιβλιοθήκη Baiduinical Manifestation
• 1. Many patients complain about mild to moderate headache after CRV, while the headache for CHS are are typically severe, ipsilateral, pounding and migrainous in type, although in some patients they may be mild, intermittent, or even absent. • 2. The neurological deficit is usually cortical (e.g. hemiplegia, neglect, hemianopia, aphasia), however, symptoms for posterior circulation ischemia (dizziness, dystaxia e.g) are not common. • 3. Seizures may be focal or generalized. Features of increased intracranial tension such as vomiting are common.
Pathophysiology:normal perfusion pressure breakthrough
• This hypothesis contains three keypoints: (a)In a healthy individual, cerebral blood flow remains relatively constant while BP varies between 80-180mmHg. When BP is low, the arteriole will relax, while BP is high,it will contract. Only in scenes of malignant hypertension, perfusion pressure breakthrough can happen. (b) Chronic cerebral hypoperfusion due to critical stenosis leads to production of vasodilatory substances such as carbon dioxide and nitric oxide,causing endothelial dysfunction (c) Correction of critical stenosis causes rapid and large changes in CBF leading to vascular disruption and ICH. Extremely large increases in CBF following CEA occur only in patients with severely impaired autoregulation, even when blood pressure is normal.
Epidemiology
• Asymptomatic increase in ipsilateral cerebral blood flow (20–40% over baseline) happens in most patients after CEA and CAS. It peaks within 24 after operation, lasts 35d. However for CHS, it often peaks at 4-5d, lasts 1-2 weeks. • Moulakakis et al reviewed 13 articals of CHS after CEA (4689 cases) and 9 articals of CHS after CAS (4446 cases) and demonstrated the incidence of CHS after CEA was estimated to occur in 1.9%, with ICH occurring in 0.37%. After CAS, CHS was estimated to occur in 1.1%, with ICH occurring in 0.74%. • CHS can also happen in other operations,such as EC-IC bypass surgery, cerebral AVM resection. A study reported as high as 15% incidence after EC-IC bypass for mymomymo patients.