Occlusion of more than 65% of the
ICA require surgical intervention.


The diagnosis of extracranial carotid artery stenosis offers the possibility of medical or surgical treatment (or both) to prevent a stroke. In about 85 percent of patients undergoing carotid endarterectomy, it was found that the combination of (1) carotid noninvasive studies, (2) magnetic resonance imaging (MRI) of the head, and (3) magnetic resonance angiography (MRA) of the head and neck satisfactorily defines carotid atherosclerosis and the cerebrovascular system. In complex cases, digital subtraction angiography is needed to image the pathologic abnormalities and the vascular anatomy.


The indications for carotid endarterectomy have been controversial until recently. Several major controlled studies confirm a highly beneficial protection against stroke in symptomatic patients with severe ICA stenosis.




There is good evidence that transient ischemic attacks (TIAs) that include either transient monocular blindness (TMB) or transient hemisphere attack (THA) are related to carotid atherosclerosis. Data indicate that significant stenosis (lumen <2 mm) or occlusion in the region of the common carotid artery (CCA) bifurcation or proximal internal carotid artery (ICA) is present in approximately 50 percent of the patients with TIAs in the territory of the carotid artery, while this is true in less than 10 percent of patients with stroke due to nonischemic cerebral disease. In addition to the 52 percent of patients with significant carotid stenosis or occlusion,6 percent have ulceration that may have been important in the symptomatology. When a patient has both THA and TMB, there is a very high probability of finding significant carotid atherosclerosis.


In patients with significant carotid atherosclerotic disease, TIAs may be caused by embolism arising from an atheromatous carotid lesion or from reduction in cerebral blood flow (CBF). It seems less likely that reduced CBF is caused by transient carotid occlusion, systemic reduction in blood pressure, or other factors.


When TMB is present, it has been suggested that embolism is the cause because of the observation of embolic material in retinal vessels. This pathologic mechanism can cause the wedge-shaped visual defects typical of central retinal artery branch occlusion, but this is an uncommon clinical finding. The common shade or curtain altitudinal symptoms suggest reduced circulation to the posterior ciliary arteries or circle of Zinn, an arterial network that could be occluded by emboli but is more likely to be susceptible to the effects of hypotension and diminished blood flow.

The patient with a THA whose angiogram shows a normal carotid bifurcation or only minimal atherosclerosis and who has an intracranial branch occlusion is likely to have a cardiac embolic source. In 25 percent with THAs had intracranial branch occlusion on angiography. The actual incidence is probably even higher because embolic occlusions are often transient. When significant carotid artery stenosis is present, THA is probably due to inadequate distal perfusion in most cases, but what part emboli play has not been established.

There is also the possibility that lacunar disease may be the cause of TIA. This diagnosis has been considered because of the pure motor or sensory character of some THAs, features characteristic of the lacunar stroke, and the finding that TIAs may precede pathologically documented lacunar infarction.


Indications for Surgical Treatment


Here will be considered the indications for surgical treatment in patients with clinical syndromes due to carotid atherosclerosis and various combinations of angiographic abnormalities in the region of the carotid bifurcation.


TIAs with Unilateral Carotid Stenosis and/or Ulceration


Carotid endarterectomy is usually indicated for the patient with TIAs and severe stenosis (>70 percent or lumen < 2 mm in diameter), and/or severe ulceration in the CCA bifurcation region or proximal ICA. These attacks are warnings of possible impending disaster. Removal of the pathologic lesion not only stops the attacks but reduces the chance of a future stroke. Controlled studies prove that for the patient with severe carotid stenosis and TIAs, carotid endarterectomy is associated with much less risk than the natural history of the disease or than medical therapy. Moreover, the more severe the stenosis, the greater the benefit of surgery. Overall, surgery confers dramatic benefit for patients with TIAs and severe stenosis.

If the studies show severe ICA stenosis with reduced flow or a thrombus in the lumen, or if the clinical picture includes increasingly severe attacks in the preceding days, attention should be directed to performing the operation as soon as possible. If there is going to be a delay, the patient should be heparinized.

If ulceration is found with a nonobstructive plaque, a decision regarding surgical or medical therapy is made based on the severity of the lesion. In the past, carotid endarterectomy has been recommended for patients with TIAs who were found to have an area of ulceration, even though the lumen diameter was greater than 2 mm. When the ulceration is deep, surgery is the recommended treatment. There is some evidence that a shallow ulcer associated with nonobstructive atherosclerosis may have a low risk of future stroke. Such patients may be treated with antiplatelet therapy and be followed with noninvasive studies of the carotid circulation. Should there be evidence of the development of stenosis or should TIAs continue. then surgery is indicated.


TIAs with Bilateral Carotid Stenosis


In some patients who are studied because of symptoms due to stenosis in one carotid artery, significant narrowing of the carotid artery is found on the opposite side. Occasionally a patient may present with a history of TIAs related to both carotid arteries. Noninvasive studies can help the physician decide the hemodynamic significance of the lesions.

When only one side is symptomatic, it is generally treated first unless the asymptomatic side has a tighter stenosis with a more severe hemodynamic lesion as demonstrated by MRA and noninvasive tests. If both sides are symptomatic, the side with the more severe hemodynamic lesion is operated upon first. The second side is usually done within 7 to 14 days. When the second stenosis is very severe, heparin therapy may be indicated until the second operation is performed.


TIAs with Ipsilateral Carotid Stenosis and Contralateral Carotid Occlusion


Most patients with this combination of lesions present with TIAs related to the internal carotid stenosis. Occasionally patients will have had neurological symptoms related to the contralateral carotid occlusion.

The indications for surgery are the same as for TIAs associated with unilateral carotid stenosis. The patient with a contralateral occlusion is more likely to have an electroencephalographic (EEG) change and need a shunt at the time of the carotid occlusion for the endarterectomy than is the patient with an open contralateral ICA. However, our experience as well as that of others is that there is no increase in neurological complications in this group.


TIAs with Tandem Stenosis


In a few patients with TIAs, angiography or MRA will show the stenosis at the carotid bifurcation or proximal ICA and a second stenosis in the intracavernous or intracranial portion of the ICA. The occurrence of this problem emphasizes the importance of complete angiography. Usually the stenosis in the neck is more severe than that found in the more distal lesion. If the stenosis in the neck is less than 2 mm, carotid endarterectomy is indicated for TIAs even if the distal lesion is also severe. Postoperatively, a decision is made between anticoagulation or antiplatelet therapy and follow-up noninvasive and MRA studies. In general, the plan has been to consider bypass surgery only in the rare case with symptoms persisting after carotid endarterectomy and a good program of medical treatment.


TIAs with Ipsilateral Internal Carotid Occlusion and the Problem of External Carotid Stenosis


TIAs can occur in the territory of a completely occluded ICA. The cause of symptoms may be an embolus from the distal end of the occlusion, an embolus passing through the external carotid circulation from atheromatous stenosis of the external or distal CCA or from the stump proximal to the occlusion in the ICA, or a reduction of flow to the eye and/or cerebral hemisphere.

Studies should include angiography of the collateral circulation through the opposite carotid artery, in many cases the vertebrobasilar circulation and lateral serial films of the head and neck over several seconds to determine the collateral flow and to see how far down the ICA the contrast agent flows. This is important in deciding about the cause of the symptoms and the probability of reopening the complete occlusion. If the angiogram shows retrograde flow below the carotid siphon, and especially if this is present to the base of the skull, there is a good chance of reopening the ICA with surgery.

If the occlusion of the ICA extends into the carotid siphon, a decision has to be made either to attempt to reopen the ICA, to use anticoagulation, or to perform a bypass graft. In general, patients with this angiographic finding will likely have had a carotid occlusion for some time, and it is usually better not to try reopen the artery. Even if there is good collateral circulation, it is favoured anticoagulation because of the risk of embolization.

If the angiogram shows a significant proximal stump in the occluded ICA in the neck and collateral flow from the external carotid via the ophthalmic artery to the ICA, this may be the source of embolus and should be treated with endarterectomy and "stumpectomy." If there is atherosclerosis with stenosis and/or ulceration at the origin of the ECA, this may also be the source of emboli and ischemia and should be treated with surgery. When the ICA is open, external carotid stenosis or occlusion does not cause significant clinical symptoms.


Posterior Circulation TIAs with Carotid Stenosis


When there is evidence of carotid artery disease either from physical examination or noninvasive studies in a patient with posterior circulation TIAs, angiography is indicated. This should include both the carotid and posterior circulations. Carotid endarterectomy is usually indicated if the angiogram shows (1) filling of the posterior cerebral artery via the stenotic ICA, (2) filling of the posterior circulation from the ICA because of vertebral artery occlusive disease, or (3) a persistent hypoglossal or trigeminal artery. It is not convincing that carotid endarterectomy will alter vertebrobasilar symptoms unless one of the conditions noted above is found on the angiogram. When severe carotid stenosis is present with no filling of the posterior circulation from that artery, the problem is viewed as an asymptomatic carotid stenosis. The optimal treatment for this lesion is then correlated with management of the vertebrobasilar occlusive disease.


Established Stroke and Carotid Stenosis


In a group of patients we treated who had suffered a stroke and were found to have carotid disease, more than half had had a prior history of TIAs due to carotid stenosis that had not brought the patient to medical attention. Because these patients are at risk for further stroke, they should be studied. A CT scan is done to define the extent of the infarction and to look for other lesions. If there is any suspicion of carotid occlusive disease, noninvasive studies and MRA (or angiography) are indicated.

In general, the presence of severe stenosis or a deep ulcer is an indication for surgical treatment. If the angiogram shows a thrombus in the lumen or a carotid occlusion that may be reopened, then surgery is performed promptly. In those patients with a recent stroke who are continuing to show improvement, and if prompt surgery is not indicated from the angiogram, operation may be delayed to allow recovery from cerebral ischemia. How long one should delay has not been established. Some have advocated waiting several weeks to reduce the chance of postoperative brain hemorrhage. If the neurological deficit is mild, we operate within a few days. If the deficit is moderate to severe, the patient will usually have CT evidence of an infarct. In this circumstance, we wait 2 to 3 weeks to allow maximum recovery. Surgery can then be done safely as long as there is careful control of the blood pressure postoperatively.

If the patient has had a massive stroke with a severe fixed deficit, only a CT scan is done. These patients cannot be helped by carotid endarterectomy.

An occasional patient will have a slowly progressive neurological deficit due to chronic cerebral ischemia. A CT scan excludes an intracranial mass lesion. MRA or angiography usually shows multiple-vessel occlusion. A combination of endarterectomy and bypass procedures may need to be considered.


Acute Stroke with Carotid Stenosis or Occlusion


If the history and/or findings suggest carotid disease in a patient with increasing TIAs in preceding days, the sudden onset of a mild to moderate neurological deficit with or without prior TIAs, or a progressive or fluctuating neurological deficit, immediate MRA and noninvasive studies are indicated. In many cases, conventional angiography will be needed for clarification. If there is severe stenosis with delayed flow, a thrombus in the lumen distal to the stenosis, or carotid occlusion with reflux to the intrapetrous segment of the carotid artery, surgery should be done promptly to allow maximum blood flow to ischemic brain tissue, prevent extension of a thrombus, and remove a source of embolization. Information from several experienced centres suggests that results of surgery are superior, but there are as yet no controlled data. A stenosis with a residual lumen diameter greater than 2 mm (not hemodynamically significant) or ulceration in a plaque at the carotid bifurcation suggests an embolus as the cause of the problem, and the patient should be considered for anticoagulation. If an acute neurological deficit occurs with loss of a previously documented carotid bruit, emergency endarterectomy should be undertaken without CT or angiography. With the careful control of postoperative blood pressure, the risk of postoperative intracerebral hemorrhage is very low.

When there is the sudden onset of a severe neurological deficit that persists, it is likely that significant infarction has occurred. This is almost certainly the case if there is a decreased level of consciousness. In this situation, restoration of blood flow by emergency carotid endarterectomy has only rarely been beneficial.


Asymptomatic Carotid Stenosis

Reliable guidelines for the management of an asymptomatic carotid bruit have not been established. Consequently, controversies exist as to the value of anti platelet or anticoagulant therapy and the indications for carotid endarterectomy. No data are available on the impact of antiplatelet or anticoagulant therapy on the eventual stroke rate in patients with asymptomatic bruit. A recent report suggests that carotid endarterectomy reduces the risk of stroke for patients with asymptomatic carotid stenosis of 60 percent or more, but only if the perioperative risk is 3 percent or less.

At the present time, it is recommended to perform MRA and noninvasive studies in those medically stable patients with an asymptomatic carotid bruit. If there is a very severe stenosis (residual lumen of 1.5 mm or less), it is strong to consider endarterectomy. This recommendation is strengthened by definite evidence of progression, reduced oculoplethysmographic values, or reversal of flow in the ipsilateral A1 segment of the anterior cerebral artery -all ominous signs of impending occlusion and possible infarction. If the noninvasive tests do not demonstrate a hemodynamic lesion and the clinical assessment of the bruit is not worrisome, it is recommended that the patient be followed on aspirin (650 mg bid) and that the noninvasive tests be repeated at 4- to 6-month intervals.

Preoperative Medical Evaluation

Many patients with carotid artery atherosclerosis have significant. medical risk factors. These include symptomatic coronary artery disease, myocardial infarction within 6 months, severe peripheral arterial disease, rheumatic heart disease, congestive heart failure, severe hypertension (blood pressure> 180/110 mmHg), and chronic obstructive pulmonary disease. Other factors to consider are diabetes, hyperlipidemia, and obesity. Previous publications have documented that the operative risks are higher in certain groups of patients with significant medical risk factors. In patients without significant risk factors, the combined operative morbidity and mortality is 1 to 2 percent. The major medical risk relates to cardiac disease, and when this is present, the operative risk is significantly higher.


Whenever there is a concern about the patient's cardiac status, a cardiologist is called for consultation. Often a thallium-persantin exercise tolerance test will be performed; evidence of significant myocardial ischemia represents a relative contraindication to surgery. In some cases, coronary angiography may be recommended, and adverse findings may suggest monitoring with a pulmonary artery catheter or even deferral of endarterectomy. Occasionally, severe symptomatic coronary and carotid occlusive disease may warrant a combined coronary artery bypass and carotid endarterectomy.


Many patients will be on several drugs for treatment of the factors noted above. In general these drugs are continued. Patients receiving diuretic medication should have the serum potassium value checked prior to operation, and any deficiency should be treated. It is important that patients with severe hypertension be treated because the incidence of postoperative hypertension and morbidity is higher in this group. This is particularly true for those patients who have an associated cerebral infarction and are at risk to develop a cerebral hemorrhage.


Other indications for intraoperative monitoring with a pulmonary artery catheter include left ventricular failure, a recent myocardial infarction, severe mitral valvular disease, and persistent angina after a coronary artery bypass. Patients with symptomatic heart block undergo placement of a temporary intravenous pacer.


Carotid Endarterectomy


Anaesthetic Management


Preoperative medication is kept to a minimum because of the fragile cardiovascular state of many of these patients. Preferable, general endotracheal anaesthesia. This technique provides good airway control, maintenance of normal arterial blood gases, maximum patient comfort, optimal surgical exposure, and some protection against cerebral ischemia.


On a few occasions,  carotid endarterectomy is undertaken with regional block in patients with a strong medical contraindication to general endotracheal anaesthesia (severe pulmonary or cardiac failure). This can be done successfully, especially in a cooperative patient, but the precision of surgery is reduced, especially when ischemia leads to movement in an agitated patient.


A radial intra-arterial cannula is inserted percutaneously for direct blood pressure recording and for blood gas measurement. The Paco2 level is kept between 30 and 39 mmHg. If there is any indication of low blood volume or hypotension, central venous pressure (CVP) is monitored, and the patient is given fluid or colloid to raise the CVP to 8 to 10 cmH2O. A vasopressor intravenous (IV) infusion is prepared, usually with 10 mg of phenylephrine hydrochloride in 250 ml of saline, and administered through a paediatric microdrip set as needed to maintain an adequate blood pressure.


Brain Protection and Monitoring


The best method of maintaining adequate cerebral circulation during the operation is to combine the benefits of general anaesthesia with the maintenance of adequate blood volume and a normal or slightly elevated arterial pressure. At the time of carotid occlusion for carotid endarterectomy, the arterial pressure is elevated to an average systolic level of 170 mmHg if there is no cardiac contraindication.


The most effective method of monitoring the intracranial circulation during the time of vascular occlusion for the endarterectomy is continuous EEG recording with a full set of leads from both sides of the head. A high degree of correlation has been found between CBF measurements during carotid occlusion and changes in the EEG. If a significant EEG abnormality occurs, with severe slowing or loss of amplitude, a shunt should be placed promptly.


The question of whether a temporary shunt is indicated during carotid endarterectomy has been the subject of many articles. Some surgeons routinely use a shunt for cerebral protection. Others never use a shunt, and some use a shunt selectively when monitoring indicates a need for it. The use of a shunt carries with it a possible risk of embolization and of injury to the intima, although rarely seen, and it does make the technical removal of the distal end of the plaque in the ICA a little more difficult. Everything should be done to reduce the morbidity of the operation to as low a level as possible. Every patient should be monitored. In only a small percentage of patients will a shunt be needed (about 10 percent in some series), but when it is indicated, it should be used. In some patients, the surgeon will know preoperatively that a shunt will be needed. These include patients in whom the vertebrobasilar circulation depends on the carotid artery or in whom there are multiple occlusions of major extracranial vessels.


Operative Technique

The patient is placed in the supine position with a thyroid bag inflated under the shoulders. The head is extended slightly, placed on a firm head holder, and turned away from the side of the operation. The opposite calf (if nonischemic) is prepared and draped for possible saphenous vein harvesting. The entire operation is done using a headlight and magnifying loupes, with use of microsurgical instruments for improved precision of plaque removal and arteriotomy closure. We prefer loupes and a headlight for greater mobility and an improved line of sight up the internal and external carotid arteries, especially with a high-lying bifurcation and plaque.

Some surgeons have recommended the use of the operating microscope for carotid endarterectomy. This may prove to be especially valuable for more proximal lesions in which the oblique upward line of sight is not important. Whether loupes or the microscope are employed, meticulous endarterectomy and closure are crucial.

The incision is made along the lower anterior border of the sternocliedomastoid muscle and just below the level of the angle of the jaw and should be curved over the muscle posteriorly and superiorly toward the mastoid process. If necessary, this incision will allow maximum exposure to the base of the skull and helps avoid retraction on the lower branch of the facial nerve near the angle of the jaw.

After the initial incision and throughout the exposure, careful attention is paid to meticulous haemostasis. This is done to permit nonreversal of intraoperative heparinization and postoperative continuation of heparinization, in most cases. To avoid unwanted bleeding, bipolar cauterization of all bleeders, even to the most minute, is recommended.


After the skin incision is made, the platysma is incised. The external jugular vein is ligated, small transverse cervical nerves divided, and the great auricular nerve identified and spared at the upper end of the exposure. Deep dissection is continued along the anterior border of the sternocliedomastoid muscle. Self-retaining retractors are used to aid the exposure. The medial blades must be kept on the subcutaneous tissue and platysma. If they are placed too deeply against the paratracheal muscles, there may be tracheal and nerve injury.


The internal jugular vein is identified just medial and deep to the sternocliedomastoid muscle. The dissection then extends along the medial border of the internal jugular vein; medial draining branches are ligated as necessary. The descendens hypoglossal nerve is often seen in the tissue just medial to the internal jugular vein and overlying the CCA. This nerve is reflected medially.

By opening the carotid sheath, the CCA is exposed medial to the internal jugular vein in the lower part of the incision. A vascular loop is placed around this vessel, which maintains its exposure and facilitates the further dissection. On rare occasions the vagus nerve lies anteriorly on the CCA, and one must be alert for this possibility.


The dissection is then extended superiorly along the medial border of the internal jugular vein. The descendens hypoglossi is kept medially and leads one to the hypoglossal nerve, which may swing low into the neck across the carotid bifurcation or lie high beneath the edge of the posterior belly of the digastric muscle. Sometimes it lies just beneath the common facial vein and may be adherent to this vessel. In some patients, nerve branches will come around the lateral side of the CCA to enter the descendens hypoglossi. Usually these branches are from the cervical plexus, but on rare occasions they seem to come from the vagus nerve. Vagal branches are preserved; they may be laryngeal. The descendens hypoglossi may be sacrificed for better exposure, without noticeable loss of function. This branch may be confirmed when bipolar stimulation causes contraction of the strap muscles (this is possible only when one or two twitches are evident on twitch monitoring). To give adequate exposure it may be necessary to remove a group of lymph nodes that are commonly present over the region of the carotid bifurcation.

When the carotid bifurcation is exposed, the region of the carotid sinus is blocked with lidocaine hydrochloride to avoid a carotid sinus reflex bradycardia and hypotension. Care is taken to leave the region of the distal common carotid artery, carotid bifurcation, and proximal ICA adherent to the posterior tissue. This avoids undue manipulation of the area, reducing the possibility of dislodging an embolus, lessening the chance of carotid sinus stimulation, and avoiding possible injury to the superior laryngeal nerve.

The superior thyroid artery is identified on the medial wall of the distal CCA or proximal ECA and a mini loop is placed around it. The ECA is exposed to the level of the first major branching of this vessel, and a maxiloop is placed at this point. If the arteriogram shows an ascending pharyngeal artery coming off the region of the bifurcation, this will have to be exposed and controlled separately.


The distal ICA is carefully exposed, staying in the tissue plane between the hypoglossal nerve or descendens hypoglossi medially and the internal jugular vein laterally. If one follows these guidelines, the distal ICA can be nicely exposed. As the hypoglossal nerve swings medially, an arterial branch often comes across the inner side of the curve of the nerve and passes posteriorly. This fairly constant sternocliedomastoid artery, often accompanied by a vein, is ligated. The hypoglossal nerve can, if necessary, be reflected gently medially with a 4-0 suture through the transected descendens hypoglossi stump. If the carotid bifurcation is located high in the neck, dissection is carried along the medial border of the internal jugular vein and beneath the parotid gland. Up to 2 cm of distal ICA exposure can be obtained by dissection of the posterior belly of the digastric muscle, with firm retraction by a Cushing retractor attached to the drapes by elastics and an Allis clamp. (The drapes are clamped with towel clips to an IV pole which is stabilized by sand bags under its wheels.) Subluxation of the jaw by wiring of the teeth can give an additional I to 2 cm of distal exposure in selected cases. It may be necessary to retract the posterior belly of the digastric muscle. On occasion the occipital artery must be divided to free the hypoglossal nerve in order to expose the distal ICA. The exposure of the distal ICA is carried to a point at least 1 cm above the distal end of the plaque. In the majority of cases the atheromatous plaque extends several millimetres further up the posterior wall of the ICA than it does on the anterior wall. Great care is taken in exposing this vessel to avoid any undue pressure or manipulation of the artery. The vagus nerve may be closely adherent to the posterior wall of the artery; occa­sionally it will be lateral or superficial to the artery. It must be carefully dissected free before placing the loop around the vessel. Pump tourniquets are placed on the loops on the common and ICAs to use in case a shunt is needed.


With a marking pen. the proposed arteriotomy is marked on the common and ICAs. The line is smooth and stays lateral. away from the bifurcation. Marking in this way avoids zigzag cuts if the arteriotomy is extended later on. A mark is made for a possible external carotid arteriotomy. Transverse hash marks are made at the expected distal end and distalmost possible end of the arteriotomy, and the external diameters are measured.

If the distal artery is very small «4 mm in diameter). or if there is a tendency to kink (or if severe irregularity of the wall is disclosed after endarterectomy). we believe there is a higher likelihood of thrombosis, which warrants selective placement of a saphenous patch graft. Therefore, in case of a kinked or very small distal ICA, it is preferable next harvest the saphenous vein at the ankle.

An incision is made longitudinally about 1 cm anterior and 1 cm proximal to the medial malleolus. After the saphenous vein is identified, the incision is carried proximally at least 10 cm. Haemostasis is obtained and Weitlaner retractors are placed. The vein is marked with a marking pen. Making every effort to avoid trauma to the vein, the surgeon opens the adventitia and dissects beneath the distal vein, placing a miniloop around it. By gently lifting the vein, attachments are put on stretch and divided sharply. Two or three large side branches are ligated with 4-0 silk and divided; small branches are coagulated with bipolar current. Finally the vessel is ligated distally and proximally, and excised. It is immediately irrigated gently (from distally) with heparinized saline. With a Potts scissors, the vein is opened along the longitudinal marking and placed in a bath of heparinized saline. The wound is closed with interrupted 3-0 coated Vicryl in the subcutaneous tissue and running 3-0 nylon in the skin.

The patient is given an IV bolus of 5000 to 7000 units of heparin. The blood pressure is raised to at least 170 mmHg systolic, if there is no cardiac contraindication.

The common carotid artery is then occluded with an appropriate vascular clamp (usually an angled Fogarty hydro-grip), care being taken to avoid injury to the underlying vagus nerve. We prefer to use Sugita temporary aneurysm clips to occlude the other arteries, but on occasion a large ICA or ECA will require the use of a small bulldog clamp. Care must also be taken to avoid injury to the vagus nerve at this point because it lies in the tissue adjacent to the ICA. The clip on the ECA is placed at or just below the first major bifurcation.

A longitudinal incision is made along the previously placed mark in the distal CCA with a no. 15 knife blade. The incision is carried through the wall of the artery until the shiny yellow surface of the atheromatous plaque is seen. A Penfield no. 4 dissector is then used to develop the plane between the atheroma and the outer arterial wall. Often the atheroma is adherent to a relatively thin outer wall at the bifurcation. It is best to separate the plaque for a few millimeters and then extend the incision superiorly with a Potts scissors before attempting further dissection. The distal end of the incision extends up the ICA to approximately the distal end of the plaque. The proximal extent of the arteriotomy is usually I to 2 cm below the bifurcation. A thin layer of thickened intima will usually extend proximally in the common carotid artery and does not need to be of concern as long as one is proximal to the stenosis.

The atheromatous plaque is then separated carefully from the outer arterial wall in the CCA. A right-angled clamp is placed around the plaque, and the plaque is cut off and bevelled with curved microscissors at the proximal end of the arteriotomy in the common carotid artery. The plaque is kept intact and is removed first from the origin of the superior thyroid artery and the proximal ECA. In some patients it is necessary to temporarily open the clamp on the ECA to remove the plaque, which may extend quite far distally. Additional bits of atheroma may be removed circumferentially with a Jacobson haemostat. The line of sight provided by loupes and a headlight is very helpful for this step. Once this removal has been accomplished, the atheroma is carefully dissected from the outer wall of the ICA, keeping gentle traction on the intact plaque. Often there is a very clean dissection plane. Great care is taken as the distal end of the plaque is reached. Usually the plaque will extend distally several millimeters further along the posterior wall of the artery. Care must be taken to remove this portion of the atheroma. Once the plaque has been separated, it usually comes away cleanly at the junction with normal intima and does not leave an intimal flap.

The plaque may "feather" away from the wall, becoming ever thinner, then vanishing. Or it may extend along the posterior wall like a yellow tongue, with a clear-cut dissection margin. In both of these situations, there is no tendency to distal irregularity or intimal flap formation. Sometimes the plaque seems to extend further distally, without a clear-cut margin. In this case the surgeon should consider a circumferential bevelling incision of the thin plaque with the curved microscissors. When done properly. this results in a very smooth inner wall, without a significant shelf effect. Tiny distal irregularities, either longitudinal or transverse, may be excised flush with the microscissors (more cleanly than by avulsion). The distal artery is inspected under loupes or microscope, with jets of irrigation to reveal any possible tendency to intimal flap formation. Further revision of the endarterectomy margin can be made. Only occasionally do we use 6-0 double-armed tacking stitches to improve such a situation.

The area of the endarterectomy is irrigated with heparinized saline and inspected with the help of the headlight and magnification. There are almost always some loose fragments adherent to the wall, which are excised or removed by peeling them in a circumferential fashion with a Jacobson haemostat. The final inspection is made of the distal end of the endarterectomy in the ICA and ECA. visualizing the area directly using a headlight and fine suction.

The arteriotomy is then closed with a continuous 6-0 Prolene suture beginning at the distal end of the arteriotomy on the ICA and progressing down onto the CCA. The 6-0 suture permits very thin bites and interbite distance (0.3 to 0.4 mm) with virtually no arterial narrowing. To avoid fracture. the surgeon should never handle the brittle suture with instruments. Seven tight square throws are needed on the distal knot to prevent untying. The suture must be snugged down with each stitch to maintain a taut suture line. Each stitch must include, under direct vision, both the medial and intimal layers on both lateral and medial sides. As one reaches the bifurcation, the lumen becomes larger and the wall thicker, and a larger bite and interbite distance (0.6-0.8 mm) are appropriate. In the CCA, a 10 to 12 mm artery warrants even larger bites and intervals (1.0 to 1.2 mm). Just before the final sutures are placed, backflow is allowed from both the ICA and the ECA so that air and any debris are flushed out of the area of the endarterectomy. If the backflow is poor, the arteriotomy is reopened and the problem corrected. In this situation there may be an intimal flap or narrowing at the distal end of the suture line. After the last suture is placed, backflow through the superior thyroid artery is permitted to exclude air from the lumen during the final tying of the suture. When the closure is completed, a rubber dam is placed over the suture line and held by a sponge with gentle pressure. Blood flow is allowed first into the ECA to wash out any further residual debris. and then into the ICA. Bleeding from the suture line is usually not a problem and is easily controlled by gentle pressure on the rubber dam. One should not be in any hurry to close small areas of leak from the suture line because most will clot with gentle pressure and patience. Surgicel is placed on the suture line. If the hemorrhage persists, the surgeon may place an additional stitch at the point of leakage, with tiny bites to avoid narrowing: a small flap of periarterial tissue may be used.

Once flow has been re-established. the endarterectomy site is checked. The exposed arteries and the superficial temporal artery are palpated gently. If there is a thrill in the ICA. the clamps are replaced and the artery reopened to correct the problem. If one is concerned about narrowing of the internal carotid lumen, a patch can be used. If there is a poor pulse or thrill in the ECA or if the STA is absent, the ECA may be obstructed. Microdoppler may be used for confirmation in that a separate arteriotomy and endarterectomy may be needed.

Not reversing the heparin may protect against thrombus formation, particularly during the first hour after the closure. Occasionally with extended cross-clamping of over 1 h, additional heparin may be needed. Rarely, bleeding at the time of closure demands (partial) reversal with protamine sulfate.

Activated clotting time (ACT) determinations during carotid endarterectomy is performed. Because the test is done in the operating room by the anaesthesiologist, with results within 5 min, data can be used to guide repetition of heparin administration or the use of protamine sulfate.

Ready vac drain No 10 is left for 24 hours. If the dressing is dry in the recovery room, heparin is restarted at 500 units/h for 48 hours. This program seems to reduce the risks of embolization and with this protocol wound haematoma is rare.


Special Technical Problems


Insertion of a Patch Graft


With the routine use of magnification for the endarterectomy, we have found that in most cases the arterial incision can be closed with a continuous 6-0 Prolene running suture. When the ICA appears to be too small for satisfactory closure (~4 mm in diameter) or it appears that closure will compromise the lumen (particularly with a tendency to kink or with a markedly irregular wall), we have no hesitation in using a patch graft. In most patients with recurrent stenosis, a patch graft is used because of the scar formation in the wall of the artery. Some surgeons use a patch routinely.


The patch is made from a collagen-impregnated knitted Dacron graft. This graft material is convenient, handles well, avoids needle hole leakage, and has not been associated with blow out. The patch is cut to fit the arteriotomy. The graft is usually about 4 mm in width near the distal end and tapers over 6 to 8 mm to a blunt distal end and gradually to a long 2-mm tail.


Double-armed sutures of 6-0 Prolene are used. One arm of the suture is placed through the distal end of the graft from the inner to the outer surface and the other arm is placed at the distal end of the arteriotomy from inside the lumen to the outer wall. Sutures are placed from the outside through the graft and then from the arterial wall lumen to the exterior, in order to accurately suture the intima and media. Four to five sutures are placed on one edge, then a similar number on the other to maintain smooth symmetry. Note that one edge will be done backhand. The graft should extend about 8- to 10-mm above the end of the remaining thickened intima to confer adequate expansion of the lumen at this critical spot. Note that in placing a patch graft, the bite size and interbite distance are larger (about 0.8 to 1.0 mm) than in primary closure. This is done to exclude the irregular wall edge from the lumen, and it can be done so because the patch offers extra material for adequate lumen maintenance. When suturing reaches the bifurcation, the tail of the graft is pulled taut and transected. The end of the patch is sewn to one side of the arteriotomy and tied. The other limb of suture is used for continuous closure of the CCA. If there is concern about a possible blowout, a 10-mm diameter Gore-tex sleeve is placed around the entire graft and carotid artery.

Use of a Shunt

When the EEG demonstrates ischemic changes after cross­clamping (slowing, voltage loss), these can be reversed to prevent stroke by the use of a shunt. However, a shunt can cause intimal dissection or emboli, which can cause a stroke. Meticulous technique can prevent these problems.

Argyle carotid shunt catheters are in common use. The advantage of these sterile polyethylene catheters is that the surgeon has four sizes (nos. 8, 10, 12, and 14 French) immediately available that are the correct length (15 cm) and have smooth ends. Shunts are prepared by filling with heparinized saline and temporary cross-clamping with a haemostat. After arterial clamps and clips are placed, a rapid arteriotomy incision is made. including through the plaque, starting a few millimeters more proximally on the common carotid artery than usual and extending a few millimeters more distally on the ICA. The shunt tube is first passed distally into the ICA; the surgeon visualizes the intima distal to the plaque so that a flap is not dissected by the tip of the catheter. A tape and tourniquet gently keep the arterial wall snug around the shunt. Rarely a Sundt-Kees clip graft can be used to provide a better view higher up. The shunt is checked to be certain there is satisfactory backflow of blood. The catheter is again temporarily occluded and is then passed proximally into the CCA, and the tourniquet is "tightened. The plaque can then be dissected and removed as previously described. Great care is taken to ensure a smooth ending to the plaque removal. especially at the distal end. Sometimes the shunt will have to be removed temporarily to ensure a satisfactory margin. The arteriotomy is closed with two sutures that begin at either end. All but about 3 mm in the central portion of the arteriotomy is closed. The catheter is clamped and removed, and the closure of the arteriotomy is completed.


Complete lCA Occlusion

When the angiogram indicates a complete ICA occlusion, changes in the operative approach are indicated. Great care is taken to avoid hypotension. An incision is made on the ICA distal to the plaque after occluding the common and external carotid arteries. In the majority of patients a thrombus will be found. but in a few the lumen of the ICA will be open distal to the atheromatous plaque. If there is a long-standing occlusion, the artery may be a firm fibrous cord without backflow, and ligation with 0-0 silk is indicated.

If the thrombus can be removed and backflow established. the endarterectomy is completed as described. In some patients with complete occlusion of the ICA, the ECA may supply significant collateral flow to the brain. In some of these patients, flow can be maintained in the ECA by the application of a Satinsky clamp across the bifurcation at the origin of the ICA or by the use of a common to external carotid artery shunt.

Certain techniques may help in opening the completely occluded artery. If a thrombus is encountered in the ICA, an effort is made to withdraw it gradually with forceps using a hand-over­hand technique. Thrombi as long as 20 cm have been removed. If this technique fails. a smooth-ended suction catheter (a shunt tube attached to suction) is introduced into the internal carotid lumen until resistance is felt. Suction is then applied. and this may withdraw the thrombus. If this method fails. a no. 3 Fogerty catheter is passed gently as far as the base of the skull. inflated. and withdrawn. Care is required to avoid injuring the distal ICA with subsequent development of a carotid-cavernous fistula. Measurements on the angiogram from the internal carotid origin to the base of the skull may help in determining the safe length of catheter that may be inserted. An intraoperative angiogram is recommended to document restoration of flow without an intimal flap or distal thrombus. If good backflow with satisfactory angiography cannot be achieved. the ICA is doubly ligated with 0-0 silk sutures. When flow is re-established, anticoagulation should be continued in the postoperative period.

Postoperative Management

Systolic blood pressure is generally maintained in the range of 100 to 150 mmHg. with efforts to avoid both hypotension and hypertension. If hypotension develops. the electrocardiogram (ECG) is checked. Mild hypotension will usually respond to the administration of IV fluid or colloid. A phenylephrine drip is available if needed. If the hypotension does not immediately respond to volume replacement, a CVP catheter is inserted. If the CVP is maintained in the range of 5 to 10 cm with judicious utilization of fluid, this problem will generally resolve. On occasion, bradycardia may develop and the administration of atropine may be necessary. The blood pressure and pulse usually return to a normal level within a few hours.

Control of hypertension is also important. There is a significant incidence of postoperative hypertension. Patients who develop postoperative systolic readings that are persistently above 170 mmHg require treatment with rapid-acting IV antihypertensive medication until long-acting medications become effective.  Intracerebral hemorrhage with postoperative hypertension was encountered. as previously reported, but since the institution of careful postoperative blood pressure control, this complication has been rare.

In most cases, we use low-dose heparin for 48 h as described and then switch to aspirin. In patients with severe irregularity of the luminal wall after endarterectomy, we use therapeutic heparinization (partial thromboplastin time, 55 to 65 s) and then warfarin therapy for 3 months (prothrombin time, 15 to 17 s). In these cases, the dissection was difficult, the endarterectomy plane seemed roughened, the plaque was particularly long, or a complete occlusion was reopened. A special circumstance when anticoagulation should probably be continued is when the patient has a severely stenotic contralateral ICA stenosis.


The mortality rate in de novo cases is 1 percent, the incidence of major stroke 1 percent, and the incidence of minor stroke 1 percent. Virtually all other patients return to their previous level of activity. Several reports of patients who have had elective carotid endarterectomies for TIAs have documented similar low morbidity and mortality rates when the operation is done by an experienced person in a center performing a significant number of operations. For patients who have had a previous stroke there is a slight increase in risk.


Reports of surgical treatment for asymptomatic carotid atherosclerosis include those of Thompson et al., who reported two strokes among 167 operations for asymptomatic bruit, and Moore et al., who reported no complications in 78 operations for asymptomatic carotid ulcerations.

Among patients with crescendo TIAs, acute mild to moderate deficit, or fluctuating or progressive stroke, enjoyed an excellent or good outcome. In this group there is 2 percent death due to a cardiopulmonary complication. There is 4 percent where the neurological deficit become worse after the operation, but there is also several spectacular recoveries in the immediate postoperative period after operation for both stenosis and occlusion. In another report of emergency carotid endarterectomy, 7 patients with crescendo TIAs all made a full recovery, and of 17 patients with stroke in evolution, none were worse, 4 were unchanged, 12 made a good recovery, and 1 died. Encouraging results in selected cases have also been reported from other centres.




Cerebral Ischemia and Infarction

The EEG electrodes are left on the patient until the patient awakens in the recovery room. If a neurological deficit is found as the patient awakens and a significant EEG change has occurred after leaving the operating room, the patient is returned immediately for exploration of the artery. If the deficit is present with no change in the EEG, a bedside ultrasound examination is performed immediately to look for occlusion and a CT scan is performed to look for hemorrhage. If these studies are normal, angiography is done. If studies show that the endarterectomy site is normal and that blood volume and blood pressure are maintained, a decision is made regarding anticoagulation. If the neurological deficit is mild and nonprogressive, usually no abnormality is found on angiography. In such patients it is assumed that an embolus was dislodged sometime during the dissection.

If the patient develops a substantial neurological deficit after an initial good recovery, it often indicates occlusion at the site of the operation. If the superficial temporal pulse is lost or the ultrasound shows occlusion, the patient should be taken immediately to the operating room to ascertain the status of the artery. If the deficit is mild and highly focal, a CT scan is done to look for hemorrhage, and if this study is normal, an angiogram is performed. The usual reason for postoperative carotid occlusion is a residual plaque or an intimal flap, but on rare occasions the problem may be associated with an ICA kink or an unrecognized hypercoagulable state.


Transient Ischemic Attacks


A small number of patients will have one or more transient ischemic episodes in the postoperative period. Usually it is a single attack, but if there is more than one it usually does not recur after 10 to 14 days and does not signify a serious problem in the operated artery.


Noninvasive studies are done to ascertain whether there is a hemodynamic lesion. Most patients will not have evidence of stenosis. They are treated with antiplatelet or anticoagulant therapy and usually do not have further problems. If TIAs persist or a significant abnormality is present on the noninvasive tests, angiography is indicated and may demonstrate a lesion that needs reoperation.


Intracerebral Hemorrhage


Typical hypertensive hemorrhage occurs in the basal ganglia 4 days after surgery when the patient's blood pressure is 200/100 mmHg. Aggressive control of postoperative hypertension reduce the incidence of this complication. However, occasionally even with a mild elevation in blood pressure, a hemorrhage may occur. Intracerebral hemorrhage is also of concern when postoperative heparin or antiplatelet therapy is used and in patients who have had previous cerebral infarction.


Cranial Nerve Injury


If the incision is carried too near the angle of the jaw or retrac­tion is too vigorous. the mandibular branch of the facial nerve can be stretched, causing weakness of the lower lip. This is an annoying problem; it causes a cosmetic change and may cause the patient to drool from the corner of the mouth. Spontaneous recovery almost always occurs. This problem is avoided by curving the incision away from the angle of the jaw toward the mastoid process and being careful with placement of the self-retaining retractors.

Injury to the vagus or recurrent laryngeal nerve with vocal cord paresis has been reported to occur in about 1 percent of patients undergoing carotid endarterectomy. Traction or pressure on the nerve is the usual cause. As noted in the discussion of operative technique, the vagus nerve can lie on the anterior surface of the common carotid artery and may be encountered early in the dissection. Another area where the vagus nerve is susceptible to injury is in dissection of the ICA, to which it may adhere. The majority of patients will show spontaneous recovery within a year.

Injury to the hypoglossal nerve is generally avoided by following the steps outlined in "Operative Technique." When it does occur, it is usually due to excessive traction on the nerve. Nothing need be done. Usually there are no symptoms, and a majority of the patients will have a spontaneous recovery within a few months.


Other Complications


Cardiopulmonary complications have been reduced by following the guidelines described under "Preoperative Medical Evaluation". Other neurological complications include seizures and headaches. When a headache occurs, it generally subsides in a day or so.

Recurrent Stenosis

Recurrent stenosis occurs in a small percentage of patients who have had a carotid endarterectomy. There seem to be three groups of patients in which this problem arises:

1.Patients in whom surgical technique has contributed to the problem. This includes failure to remove the distal tongue of the plaque, narrowing of the lumen during the arteriotomy closure, and damage to the intima by vascular clamps.

2.Patients who have a tendency to excessive scar formation.

3.Patients who develop a combination of fibrosis, recurrent atherosclerosis, and, at times, an associated thrombus.


Symptomatic stenosis may recur within a few months of the operation. This usually relates to one of the problems in surgical technique or to the thickened fibrosis of the arterial wall, which is grossly and histologically distinct from the typical atherosclerotic plaque. Fortunately, this tendency to excessive scar formation is a rare happening. Recurrent stenosis that occurs after 2 years usually has significant atheroma formation as well as fibrosis.


Reoperation is often difficult because of the dense periarterial scar and the fibrosis of the vessel wall. Great care is required to avoid injury to the internal jugular vein and the vagus and hypoglossal nerves. The thickened intima is often densely adherent to the arterial wall, particularly in the region of the previous suture line. In most patients it is necessary to use a patch graft to repair the artery. In some instances where myofibrointimal hyperplasia is the problem, no dissection plane can be developed, and patch grafting alone is the best procedure.