Keywords
carotid endarterectomy, complications, thrombosis, stroke, restenosis
Highlights
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Carotid endarterectomy is a safe, effective, and durable procedure with a complication rate approximating 2% to 4% in recent studies.
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Patient selection is the single most important factor in complication avoidance.
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Although uncommon, complications of carotid endarterectomy can be devastating unless promptly recognized and corrected.
Background
Throughout its history, carotid endarterectomy (CEA) has been a safe and effective means of preventing stroke due to carotid artery disease. The procedure was first shown to reduce incidence of stroke in patients with symptomatic carotid artery stenosis in a randomized multicenter trial in 1969. The North American Symptomatic Carotid Endarterectomy Trial (NASCET), a nonblinded, multicenter randomized controlled trial, was halted in 1991 after interim analysis of 659 patients with high-grade stenosis (>70%) revealed a 17% absolute risk reduction of ipsilateral stroke at 18 months in those undergoing CEA compared with medical management. The European counterpart to NASCET, the European Carotid Surgery Trial (ECST), similarly demonstrated an 11.6% absolute risk reduction of stroke at 3 years after surgery in patients with symptomatic, high-grade (80% or greater) stenosis. Studies have also suggested that CEA is superior to medical management in patients with asymptomatic carotid stenosis. Most notably, the Asymptomatic Carotid Atherosclerosis Study (ACAS) was a prospective, randomized, multicenter trial that enrolled 1662 patients and showed an estimated 5-year risk reduction of stroke or death of 6% in those with greater than 60% stenosis undergoing CEA compared with medical management.
CEA has remained the mainstay treatment for carotid artery stenosis because of its effectiveness, durability, and low complication rate. Most series report a periprocedural complication rate approximating 2.3 to 4.3. Even in the most recent trials comparing modern minimally invasive endovascular techniques, carotid angioplasty and stenting (CAS), to CEA, CEA has a safety profile equivalent to that of CAS and may be associated with a lower risk of stroke. This chapter will review the periprocedural and postprocedural complications of CEA with a focus on techniques to mitigate or avoid complications.
Anatomic Insights
Standard exposure for CEA involves dissection medial to the sternocleidomastoid muscle with dissection in an avascular plane to find the carotid sheath. This is then opened and the jugular mobilized laterally to identify the carotid artery, and the vagus nerve is identified as well. When exposing the carotid artery, one must be aware of the close proximity of a number of cranial nerves or their branches, including the vagus, the recurrent laryngeal, and the hypoglossal nerve as well as the marginal mandibular branch of the facial nerve ( Fig. 14.1 ). Cranial neuropathy has been reported at a rate of 5% to 8% according to recent multicentered trials, including CREST and NASCET. In general, these are the result of neuropraxic traction injuries which will improve or resolve with time.
The most common cranial nerve palsy is a hypoglossal nerve injury, which accounts for more than half of all cranial neuropathies after CEA, according to one recent study. The hypoglossal nerve is routinely identified during surgery because it usually crosses the internal carotid artery (ICA) and external carotid artery a few centimeters above the bifurcation. It is helpful to identify the superior root of the ansa cervicalis and follow it superiorly to its branch point from the hypoglossal. Occasionally, the hypoglossal nerve may be hidden or fixed behind the facial vein, and injury can occur when dividing the facial vein is attempted. Dissection carried along the entire length of the nerve to allow medial mobilization is helpful in preventing traction injury, as is sectioning the ansa cervicalis if the nerve is tethered.
The marginal mandibular branch of the facial nerve is also at risk during CEA. The marginal mandibular branch typically runs along the inferior aspect of the jaw and is at risk for neuropraxic injury via compression from retractors. To avoid this, retractors should be placed superficially, and care should be taken to maintain retractor blades without excessive direct compression at the angle of the jaw. If injury is encountered, patients can be reassured that this palsy typically resolves over the course of weeks to months. Clinically, marginal mandibular palsy can mimic a postoperative ischemic event but will always be ipsilateral to the CEA. A thorough neurologic examination, clearly ruling out any other neurologic deficits to exclude stroke, is of key importance when attributing facial droop to marginal mandibular palsy.
The vagus nerve lies posterolateral to the carotid in the carotid sheath and can be inadvertently injured when exposing and attempting to separate the carotid artery and the internal jugular vein or when clamping the carotid artery. Injury can lead to hoarseness, which, depending on the mechanism of injury, often recovers over the course of months. Careful identification of the vagus nerve once the carotid sheath is entered as a routine part of the exposure minimizes the risk of vagal nerve injury. The recurrent laryngeal nerve lies in the tracheoesophageal groove and is also prone to traction injury if the medial blade of the retractor is placed too deeply.
The key to minimizing or avoiding cranial nerve complications altogether lies in a solid understanding of the anatomy encountered during the exposure of the carotid artery. Armed with this knowledge, the surgeon can avoid almost all of the more serious cranial nerve injuries.
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Preoperative Risk Reduction: Patient selection
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Patients with anatomic red flags such as previous neck radiation, previous neck surgery, high carotid bifurcation, or a contralateral carotid occlusion should be carefully evaluated.
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Perioperative Risk Reduction: Intraoperative technique and early recognition
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Intraoperative monitoring techniques such as regional anesthesia with awake neurologic examination, EEG, somatosensory evoked potential (SSEP), transcranial Doppler.
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Changes in mental status or focal neurologic deficits during cross-clamp may be overcome with proper increase in blood pressure or shunting.
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Identify intraoperative carotid occlusion by backbleeding.
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Ensure there is no chance of dissection flap with careful plaque removal and inspection.
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Postoperative Risk Reduction: Early recognition and treatment
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Expanding neck hematomas demand prompt recognition and treatment at bedside with early involvement of anesthesia.
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Preventing intraparenchymal reperfusion hemorrhage postoperatively necessitates precise blood pressure management.
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Stroke can be a devastating complication of surgery, and prompt recognition is paramount because it is often reversible if caught early.
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Complication Prevention: Patient Selection
The first step in complication avoidance is appropriate preoperative patient selection. The NASCET and ACAS trials firmly established CEA as superior to best medical management for both symptomatic and asymptomatic carotid atherosclerotic disease in the early 1990s; however, medical management has improved since that time with the evolution of statins and antiplatelet drugs. CREST-2 is currently enrolling patients to answer the question of best treatment for asymptomatic carotid stenosis in the modern era. Certain patients carry a high surgical risk, such as those with previous neck radiation, previous carotid disease, severe heart or lung disease, a high carotid bifurcation or plaque extension above C2, and/or contralateral carotid occlusion, and CAS is noninferior to CEA in this population. 2016 data shows that CAS is also noninferior to CEA for patients <80 years of age with asymptomatic stenosis ≥70%, with an experienced endovascular surgeon and use of an embolic protection device. Given the slightly higher risk of stroke in CAS and its impact on quality of life, CEA may be preferred over CAS in symptomatic patients without high surgical risk factors.
Perioperative Complication Prevention and Management
Dissection Flap
It is imperative to ensure that the plaque is removed completely with a smooth transition to the normal intima. An intimal flap can lead to dissection of blood between the endothelial and muscular layers, leading to occlusion or stenosis of the artery. This is best prevented by performing an arteriotomy of the ICA of sufficient length to allow adequate visualization and dissection of the distal end of the plaque. The plaque can usually be feathered out by careful circumferential dissection with an instrument such as a Rhoton round knife. If the plaque fragments, ring forceps should be used to ensure complete removal under magnified vision. On occasion, there may be an edge of the plaque that does not feather out and is not a completely smooth transition to normal intima. In this case, a 7-0 or 8-0 Prolene suture should be used to tack the flap at its most proximal edge. The suture knot must of course be outside the vessel lumen, which can be accomplished by using a double-armed suture. The bite must be small to prevent kinking or stenosis of the artery. At times several tiny sutures should be used, rather than one suture with a larger bite. On the unusual occasion that the plaque continues distally and maximum cranial exposure has been obtained with mobilization of the digastric belly, it may be necessary to secure the remaining plaque with a mosquito or ring forceps and sharply pull to release the plaque. Although this may cause some angst on the part of the surgeon, it has proven successful and without complication on a number of cases in our experience. Should this maneuver be required, it may be advisable to use dual antiplatelet agents for 6 weeks after the endarterectomy.
Intraoperative Ischemia
The use of shunting in CEA is a topic of controversy. Some surgeons use shunts for all cases, whereas others use this technique selectively in the case of neurologic decline. Both are well supported in the literature and are dependent on the surgeons’ training and preference.
Both methods have benefits as well as potential complications. Use of a shunt carries risk of embolization of distal debris or air as well as the risk of distal dissection as demonstrated in Surgical Rewind, “My Worst Case”. Ensuring that the artery is opened distal to the plaque and that the shunt is appropriately backbled will help prevent these complications. In 754 patients undergoing CEA with selective shunting, 32.6% had a new lesion on diffusion-weighted magnetic resonance imaging compared with 4.2% of the nonshunted patients, although 80% of these were asymptomatic.
In the case of CEA with selective shunting, a shunt is employed only if the patient develops ischemia with impairment of neurologic function during the period of carotid cross-clamp. Numerous monitoring techniques for the detection of cerebral ischemia have been described. We prefer a neurologic examination in a patient who is awake and under local anesthesia due to its high sensitivity and specificity for ischemic impairment. This may manifest as alteration in level of consciousness, agitation, hemiplegia, or aphasia. Other techniques such as EEG, SSEP, or transcranial Doppler have also been successfully employed for monitoring patients under general anesthesia. During temporary carotid occlusion, maintaining systemic blood pressure between 160 and 200 systolic, or 20% above baseline, can help maintain perfusion through the maximally dilated vasculature of the ischemic brain. Ensuring careful dissection around the carotid body can help prevent bradycardia and hypotension, which can be augmented by the injection of local anesthetic into the carotid body. Preoperative recognition of the patency of the anterior communicating or posterior communicating arteries can help predict whether a shunt will be needed; however, in the senior author’s experience (JAW) using regional anesthetic, 4.9% of patients required shunting (n = 325, unpublished data). In fact, only 23.3% of patients with a contralateral occlusion required shunting in this series. Prior to incising the carotid, neurologic testing should be performed after 30 to 60 seconds of ICA clamp time. A carotid shunt should always be immediately available, and the surgeon and surgical team should be familiar with its use.
Intraoperative Carotid Occlusion
Intraoperative carotid occlusion is a potentially catastrophic complication that must be recognized promptly and followed immediately by corrective actions. Intraoperative occlusion is evaluated by backbleeding the ICA before final closure of the suture line, which also allows for egress of any remaining air and/or microdebris. If there is no backflow, additional heparin is given with an activated clotting time (ACT) to confirm that the patient is appropriately anticoagulated. We aim for a goal ACT of 225 to 250. The distal suture line should be immediately reopened and the lumen inspected for clot, debris, or a backwalled suture. When flow is reestablished, the ICA clip is replaced and the ICA sutured and backbled again just before the final suture is tied. If there is no flow, a Valsalva and suction should be performed with the ICA clip off to dislodge potential clot. Should this fail to result in brisk backbleeding, a 3-French Fogarty catheter can be passed distally, inflated gently, and pulled back to remove any clot, followed by backbleeding.
If the reason for thrombosis is not mechanical (i.e., a backwalled suture), addition of a second antiplatelet agent such as clopidogrel should be considered because certain patients demonstrate relative insensitivity to aspirin, with a 34% incidence of normal collagen/epinephrine closure times on PGY100 testing in patients with cerebrovascular ischemic symptoms.