Clinical studies have confirmed that carotid endarterectomy (CEA) has an unquestionable place in the management of symptomatic (stenosis greater than or equal to 50%) and asymptomatic (stenosis greater than or equal to 70%) ischemic cerebrovascular disease caused by carotid stenosis, and is an effective treatment for ischemic stroke caused by atherosclerotic stenosis of the carotid artery It has been widely accepted. From June 2001 to April 2010, 369 patients with carotid stenosis were admitted to the Department of Vascular Surgery of Changhai Hospital, and 36 of them were treated with carotid endarterectomy + embolization for complete occlusion of the internal carotid artery with symptoms. Zhao Zhiqing, Department of Vascular Surgery, Shanghai Changhai Hospital
Materials and methods
I. General information
There were 36 patients in this group, 31 males and 5 females, with a mean age of 67.6 (44-81 years). More than 83.3% of the patients had new cerebral ischemic events, including 19 cases of cerebral infarction and 11 cases of TIA. On admission, all patients had various clinical manifestations of varying degrees, mainly dizziness, dark haze, aphasia, and limb sensory and/or motor disturbances. The symptoms were limited to one side in 25 cases, of which 19 cases were attributed to carotid occlusion and 6 cases were associated with carotid stenosis on the opposite side of the occlusion, including 3 cases with bilateral symptoms. Concomitant diseases included hypertension in 31 cases, diabetes mellitus in 17 cases, coronary heart disease in 13 cases, and COPD in 11 cases. Other risk factors included smoking in 26 cases, postoperative cancer in 3 cases, and chronic renal insufficiency in 1 case. The mean time to the most recent cerebral ischemic event was 32 days (6-65 days) from surgery.
II. Methods
All cases underwent preoperative carotid ultrasound and magnetic resonance angiography (MRA) to assess the patency of the carotid arteries (including carotid and vertebral arteries) and the compensatory capacity of the willis loop, focusing on the length of the occluded carotid artery and the ultrasound echo of the filler causing the occlusion. Preoperative CT or MRI of the head was routinely performed in all patients for comparison with the postoperative examination. MRA of the carotid artery was repeated 1 week after surgery to understand the patency of the occluded carotid artery after surgery.
2.Preoperative preparation Preoperative low molecular heparin anticoagulation therapy, 0.4ml, subcutaneous injection, 1 time/day, and prostaglandin 40µg, intravenous drip, 1/day, to improve the blood supply of intracranial side branches.
3. Surgery The surgery was usually performed 4-6 weeks after the occurrence of severe cerebral ischemic events, and was performed under general anesthesia with tracheal intubation without carotid diversion tube. The occluded carotid artery was treated by carotid endarterectomy. If the patient’s preoperative MRA indicated occlusion of the internal carotid artery to the intracranial segment or there was no obvious internal carotid regurgitation after removal of the plaque, intraoperative embolization treatment with a 2F or 3F Forgarty catheter was added, and the lesion was removed and sent for pathology, and a negative pressure drainage bulb was placed to drain the incision. Postoperatively, 40 mg of low molecular heparin was administered once/12 hours and transitioned to Warfarin anticoagulation combined with antiplatelet medication before discharge. Two of the cases were admitted to the Department of Thoracic Surgery for coronary artery bypass surgery 3 weeks after surgery.
III. Follow up
The follow-up was performed by neck MRA or carotid ultrasound at 1 week and 3, 6, 12 months after surgery and annually thereafter, respectively, to adjust the drug dose and observe whether there was restenosis, thrombosis and cerebral ischemic events after surgery.
Results
1. Imaging and pathological findings.
MRA showed that the occlusion of the internal carotid artery was mainly located at the proximal end of the internal carotid artery. 7 of the 36 cases were only limited occlusion of the initial segment of the internal carotid artery, and the length of occlusion was less than 3 cm; in 11 cases, the length of occlusion was greater than 3 cm, but the stump outflow tract was still visible at the distal end of the internal carotid artery; in the remaining cases, the occluded segment reached the willis loop. Twelve cases had more than 50% stenosis in the carotid artery contralateral to the occluded carotid artery; 23 cases had old or recent infarcts as indicated by CT/MRI scan of the skull.
Twenty-eight pathological specimens were sent for examination. 17 cases had atherosclerotic plaque with red thrombus, 10 cases had atherosclerotic plaque with mechanized thrombus, and 1 case had internal carotid artery entrapment resulting in secondary thrombotic occlusion of the lumen.
2.Surgical results
Twenty-eight cases were treated with conventional carotid endarterectomy + Fogarty catheter for embolization, and 8 cases were treated with external carotid endarterectomy + Fogarty catheter for embolization. The carotid artery block time ranged from 14 to 35 min (mean 18.4 min) in all cases. In 4 cases, the internal carotid artery was ligated and external carotid endarterectomy was performed because the carotid artery thrombus was completely mechanized and could not be completely removed. 7 cases developed cerebral hyperperfusion syndrome after surgery and were treated with hormone and intracranial pressure reduction, and gradually recovered after 3 days; 1 case developed hoarseness due to intraoperative tracheal intubation, and later recovered on its own; 3 cases developed subcutaneous hematoma after surgery. One case had subcutaneous hematoma after surgery, and one case had respiratory distress due to hematoma compression, which was explored and drained for 3 days with sutures and healed well. All patients recovered well after surgery, and their speech or limb function improved to different degrees.
3.Follow-up results
All 36 patients underwent MRA or ultrasound examination 1 week after surgery, which indicated that the internal carotid artery was patent in 22 cases (68.8% patent rate) and re-occluded in 10 cases. 1 of the 22 patients died due to trauma, and the remaining patients had clear consciousness, no limb sensory movement disorder, dizziness, and faster speech and thinking than before. 10 patients with re-occlusion of the internal carotid artery and 4 patients with intraoperative ligation of the internal carotid artery had good MRA. The MRA showed good visualization of the external carotid artery. Two of them had TIA and lacunar infarction 4 months after surgery; three of them still had occasional dizziness after surgery, and two of them had unilateral limb numbness; one case had memory loss. With a mean follow-up of 15 months (February-45 months), the
DISCUSSION
Although there have been case reports of occluded carotid artery revascularization since 1958, there is still controversy among clinicians regarding the necessity of treating carotid artery occlusion. Most scholars believe that because the internal carotid artery is occluded, no blood flow through the internal carotid artery can produce emboli and cause intracranial embolism. However, clinical studies have demonstrated that cerebrovascular ischemic events can still occur after internal carotid artery occlusion, especially in patients with symptomatic internal carotid artery occlusion [1].
The incidence of internal carotid artery occlusion is about 15% in people with symptomatic (cerebral ischemia or retinal ischemia) carotid stenosis [2], and most patients with internal carotid artery occlusion have no obvious symptoms, and those with symptoms tend to present with multiple TIA episodes. The risk of stroke in asymptomatic carotid stenosis is about 2-2.5%, and most patients have coexisting conditions such as coronary artery disease and hypertension, and their risk of surgical complications is equal to or exceeds the risk of disease in the natural state; therefore, patients with asymptomatic internal carotid artery occlusion should be followed up regularly with a specialist. In contrast, patients with symptomatic carotid artery occlusion who develop a TIA have about an 11.5% chance of having a further serious cerebral ischemic event, the risk of surgical treatment is much lower than the risk of natural disease progression, and there is evidence that surgical treatment is more effective than pharmacological treatment [3]. Therefore, patients with symptomatic internal carotid artery occlusion should be treated aggressively with surgery. If a patient has an internal carotid artery occlusion with severe stenosis of the contralateral carotid artery, endarterectomy of the occluded side first should be preferred because of its low impact on cerebral blood flow and low incidence of perioperative cerebral ischemia.
The main possible causes of internal carotid artery occlusion are: 1) thrombosis at the site of severe stenosis carotid artery lesion leading to vascular occlusion; 2) hemorrhage within the atherosclerotic plaque of the carotid artery can also cause internal carotid artery occlusion; 3) thrombosis can also be caused by internal carotid artery entrapment [2]. Color Doppler ultrasound can accurately identify secondary thrombosis, intraplaque hemorrhage, and internal carotid artery entrapment by observing the morphology of carotid atherosclerotic plaque and the echo of the luminal filler. In this group of patients, there were 25 cases of atherosclerotic stenosis secondary to red thrombus, 10 cases of atherosclerotic plaque rupture with mechanized thrombus, and one case of internal carotid artery entrapment leading to secondary thrombotic occlusion of the lumen.
The pathological nature, extent, and length of the occluded segment of the internal carotid artery determined the effectiveness of surgical treatment. If the lesion is severe stenosis or bleeding within the plaque secondary to acute thrombosis, it is mostly red thrombus, and the thrombus can be dissolved and self-passed by anticoagulation and antiplatelet therapy in a few patients. However, since it takes about 2 weeks for the cerebral blood supply to self-regulate into homeostasis, the restoration of blood flow after carotid endarterectomy in patients with cerebral infarction can cause amplification of the inflammatory response in brain tissue leading to increased ischemia or hemorrhage. Therefore, for patients with definite cerebral infarction after carotid occlusion especially large cerebral infarction, it is recommended that surgery should be performed at least 1 month after cerebral infarction [4]. However, a randomized controlled clinical study found that patients with symptomatic severe carotid stenosis had the greatest benefit if they were treated surgically within two weeks of the most recent ischemic event [5]. Therefore, this principle was followed in our group of patients with carotid artery occlusion without massive cerebral infarction, and the surgical outcome was satisfactory. In contrast, chronic internal carotid artery occlusive lesions have been formed for too long, and the plaque and thrombus at the internal carotid artery occlusion have gradually become mechanized, fibrotic, and calcified, making the internal carotid artery thinner and unable to completely remove the intima of the atherosclerotic plaque, thus reducing the success rate of surgery. Since the prognosis of patients after treatment of acute internal carotid artery occlusion and chronic internal carotid artery occlusion is different, when acute carotid artery occlusion is suspected, further ultrasound and MRA should be improved to establish the diagnosis and then operate as early as possible to achieve good treatment results [3].
In the case of internal carotid artery occlusion, the blood flow may return from the collateral circulation of the skull base arterial ring to the distal end of the occluded internal carotid artery, therefore, the occluded internal carotid artery often appears as a stenosis at the beginning of the internal carotid artery and gradually worsens until the lumen is completely occluded and the blood flow is completely blocked, and then the distal end gradually reveals the outflow tract. Therefore, for patients with long internal carotid artery lesions or patients with no or unsatisfactory regurgitant bleeding after endarterectomy, a 2F or 3F embolization catheter can be used to retrieve the embolus, which can expand the internal carotid artery in the intracranial segment while retrieving the embolus, thus increasing the regurgitant bleeding and improving the success rate of surgery.
The internal carotid artery has many branches that can communicate with the external carotid artery through the meningeal artery and ophthalmic artery, which is one of the important reasons why some patients with complete occlusion of the internal carotid artery do not experience cerebral infarction. Therefore, when the internal carotid artery cannot be surgically reopened, improving the blood flow of the external carotid artery can still achieve the purpose of preventing cerebral ischemia. In our group, four patients who failed to recanalize the internal carotid artery by surgical treatment and ligated it, their symptoms improved after external carotid arterioplasty.
The surgical risk of occluded internal carotid endarterectomy is related to the extent of carotid involvement, the nature and location of the lesion and coexisting diseases such as hypertension, diabetes, chronic lung disease and congestive heart failure, and smoking. The main complications are perioperative stroke (both ipsilateral and/or contralateral to the occluded carotid artery), postoperative hypertension, cerebral reperfusion syndrome, intracranial hemorrhage, intracranial hypertension, and myocardial infarction. The intracranial blood flow will suddenly and dramatically increase after occluded carotid endarterectomy, and the preoperative capillaries, small arteries, and neurons may rupture and bleed or extravasate fluid when high-pressure blood flow passes through them due to ischemic injury. Because of the damage to the carotid sinus during carotid endarterectomy, the sinus arch reflex cannot be regulated properly, and acute hypertension will develop several hours after CEA [3]. Hypertension and increased cerebral blood flow can cause cerebral hemorrhage and cerebral edema after CEA. Thus, in patients with carotid occlusion who have hypertension, strict monitoring and control of hypertension is extremely important to prevent complications such as cerebral perfusion syndrome and intracranial hemorrhage.
Current trends in the treatment of carotid stenosis tend to be minimally invasive, and thus carotid stenting appears to have an extremely important place in the treatment of patients with severe stenosis. However, in patients with internal carotid artery occlusion, carotid stenting has limited ability to treat atherosclerotic occlusion of the lumen and old thrombotic lesions, despite the success reported [6], and CEA is an effective and safe method for the treatment of internal carotid artery occlusion.