VEITHSymposium: A Look at Complications in Carotid Artery Stenting
- Volume 22 - Issue 2 - February 2014
- Posted on: 2/1/14
- 0 Comments
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What are some of the complications that can occur in patients undergoing carotid artery stenting?
There are the complications that might occur in all endovascular treatments, like hematoma formation, arteriovenous fistula, and false aneurysm at the puncture site, thrombosis or dissection of access arteries, and adverse contrast material reactions. Most dangerous is an unrecognized retroperitoneal bleeding, which might have a fatal end. The incidence of these complications can be kept low with a good angiographic technique.
More important are the severe complications like acute occlusion or rupture of the carotid artery, brain infarction or cerebral bleeding. Operators must be familiar with all potential complications in order to avoid them or to solve the problems on the table. You should never feel too safe. The risk of complications always exists. In elderly patients who have been suffering for decades from high blood pressure, we often find elongated arteries. The access to the lesion may be demanding in these patients. The aortic arch itself may be a technical challenge. As catheters come up through the aortic arch, they can dislodge and embolize atherosclerotic material. The particles will go into the cerebral circulation or other organs.
Then there is the problem of the lesion itself. The act of crossing the lesion can cause embolization. Touching a high-degree stenosis in the wrong manner can also cause it to occlude. Then you have not helped the patient, and in most cases, the procedure will end without any success. If you are lucky, the patient will not have a stroke, but this is not predictable.
I have listed some possible vascular reactions, but many additional factors must be considered. For example, there are pressure receptors on several sites in the body, and one is on the carotid artery. The carotid body, located at the carotid bifurcation, measures the gas concentration in the blood and also the blood pressure. Carotid comes from the Greek language and means “sleep artery”. When tissue at this receptor site is compressed, it causes you to fall “asleep” due to the development of bradycardia. During carotid intervention, this compression occurs during balloon dilatation, because when the lesion is ballooned at the level of the carotid body, the pressure receptors in the tissue will react, triggering bradycardia. Normally, before we do a dilatation, atropine is given intravenously to overcome this effect. However, in some patients, especially those with reduced ejection fraction due to coronary artery disease, blood pressure may not resume to a sufficient level. These patients end up in the intensive care unit and are given medication to stabilize their blood pressure. It is not a high number — we have had three cases out of more than 5,000 — but you still have to be prepared. Our three patients had to stay several days in an intensive care unit until their blood pressure normalized.
A somewhat lower blood pressure after carotid artery stenting can be observed more frequently, and may be caused by the pressure of the self-expanding stent on the carotid body. This effect lasts sometimes for several days and is welcome because it reduces the risk of hyperperfusion.
Hyperperfusion is another possibility. Normally there is a very constant perfusion of brain tissue, independent of the systemic blood pressure. This is called autoregulation. The cerebral arteries can dilate or constrict, and in that manner, manage constant blood flow throughout the brain. When a carotid stenosis is removed, then suddenly, the systemic pressure will enter the cerebral arteries. If there is a tight stenosis of more than 80 or 90%, that means there is less than 1 mm left in the artery diameter and the risk of hyperperfusion is increased.
Beforehand, the cerebral arteries were dilated as much as possible to reduce the flow resistance and direct as much blood as possible to the brain tissue. Removing the stenosis causes a sudden, higher pressure in that system. In normal people, the cerebral arteries will constrict and so adapt again to the situation, creating a normal blood perfusion. In the elderly, some patients may need hours or even days until they have a normal cerebral flow rate again. Increased perfusion can cause cerebral edema or even cerebral hemorrhage.
Is this also a risk in carotid endarterecomy?
Bradycardia is not an issue in surgical repair, because the tissue is removed and the carotid body is destroyed. But hyperperfusion can happen in carotid surgery. Surgeons also have, from time to time, cases with cerebral hemorrhage. What must be done? First, you have to detect hyperperfusion. Patients normally complainof headache on the affected side and might later develop brain edema. The flow rate can be measured with transcranial Doppler in the middle cerebral artery. If the flow rate is significantly increased, then the blood pressure must be lowered as far as the patient will tolerate it. A systolic blood pressure of 100 mm of mercury is welcome in this situation. The patient will not have vertigo, because he is lying in bed. Blood pressure must be monitored not only during the procedure, but after the procedure as well.
We do have cases where it is better to send the patient for surgery. This is especially true for heavily calcified lesions, because the principle of balloon dilatation requires some distensibility of the arterial wall. If a thick circular calcification is present, no distensibility exists. You can put a balloon in the vessel, but either the balloon will rupture the vessel or the balloon itself will rupture. Patients also better treated by surgery include extreme elongation and tortuosity of the carotid artery.
On the surgical side, about 5% of patients seen by vascular surgeons may be better treated by endovascular means than with open surgery. This includes patients with a previous carotid endarterectomy, a neck dissection and radiotherapy for cancer disease, a paresis of the laryngeal nerve, and a bamboo spine due to Parkinson’s disease. Some patients, about 4% of the population, have a very high carotid bifurcation, which makes it more difficult for surgeons to operate and results in a much higher complication rate. Patients with tandem stenosis, who not only have a bifurcation lesion, but additional stenotic lesions in the distal internal carotid artery or the ostium of the common carotid artery, may also have better outcomes with an endovascular intervention.
In my experience, about 80% of patients could be treated either with surgery or with carotid artery stenting. The method may not be as important as who is doing it and their experience level. Trial data show about a 5-7% complication rate. But when we look into the data of participating single centers, some have a complication rate of more than 10% and others of less than 3%. If I had a carotid stenosis, I would like to be treated by a physician with less than 3% complication rate. Operators need a certain number of cases per year to be considered well trained and they must have all the devices available as well. The minimum caseload would be about 50 cases per year. If you have <50 cases, that is <1 per week, it is questionable whether you are doing any good, because we know that your complication rate will be higher than necessary.
What about embolic protection devices?
Embolic protection is essential for carotid artery stenting, because we deal with a mainly embolic disease and can cause embolization of atherosclerotic debris. Presently, filter protection and proximal balloon protection are used. When you use filters, you have to cross the lesion without protection, which imposes a risk, even when it is low. Filter devices can certainly cause problems when you don’t know how to manage them properly. When you are working with an open-cell stent design in a carotid artery that has a lot of bends, the retrieval catheter can hook on the struts of the stent. Here, technical experience and skill are necessary to cross the stented segment and get the filter out. There are some reports where operators pulled the filter, the filter hooked on the stent, they pulled some more, and suddenly, the filter dislodged and embolized — and then it is really a problem to get it out.
Dwell time for a cerebral protection device normally lasts 5-8 minutes and then the stent is placed. If the operator doesn’t have experience and needs a quarter of an hour or more, then the filter might clot, and then low flow can become an issue. Low flow can occur throughout the procedure and then at the final control angiogram, there is no blood flow in the carotid artery. In that case, the most frequent cause is that the patient has developed spasm of the internal carotid artery. The second most often cause is a full filter basket. The embolic material causes no or low flow, and so an aspiration must be done before the filter is removed. The third cause is that the filter device has spent too long in the artery, causing thrombus formation on the inner and outer surface of the filter membrane.
Medication is also important, before, during, and after the procedure, because when the patient has not been loaded with antiplatelet drugs, the embolization risk goes up. Re-occlusion after treatment must be prevented, and that is also done by medication.
Some believe that we need to open the carotid artery, not necessarily make it perfect. Perhaps a 30% or 40% stenosis still might be acceptable.
Naturally, we try to achieve a perfect result, which means a normal diameter of the carotid artery. We don’t overdilate, because that only creates problems in the vessel wall and more reaction from the tissue in the vessel wall, potentially leading to intimal proliferation. But yes, we respect a residual stenosis of 10 to 30%, because with that degree of stenosis, the patient will not develop a stroke. And the aim of carotid artery stenting is prevention of stroke!