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Carotid Endarterectomy Technique

  • Author: Omar Haqqani, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Dec 09, 2014
 

Conventional Carotid Endarterectomy

The steps in a conventional carotid endarterectomy (CEA) are illustrated in the video below.

Carotid endarterectomy: operative techniques.

Incision

A cervical incision is made parallel and anterior to the sternocleidomastoid and centered over the carotid bifurcation. This incision can be extended proximally to the sternal notch for more proximal lesions of the common carotid artery (CCA) and distally to the mastoid process for higher exposure. Its upper end should be angled posterior to the earlobe to avoid the parotid gland and the greater auricular nerve. The incision is carried down through the platysma, and the sternocleidomastoid is retracted laterally with self-retaining retractors.

Exposure and mobilization

The internal jugular vein is visualized, and the carotid sheath is opened along the anterior border of the vein. The internal jugular vein is retracted laterally, and the common facial vein is ligated. Dissection is continued anterior to the CCA to keep from injuring the vagus nerve. The vagus nerve usually lies in a posterior lateral position within the carotid sheath but occasionally may spiral anteriorly, particularly in the lower end of the incision.

Attention should be paid to cranial nerves IX (glossopharyngeal nerve), X (vagus nerve), XI (accessory nerve), and XII (hypoglossal nerve), as well as the marginal mandibular branch of VII (facial nerve) and the rare nonrecurrent laryngeal nerve that comes directly off the vagus to innervate the vocal cords. This nerve can cross anterior to the carotid artery and can be mistaken for a part of the ansa cervicalis; if it is inadvertently divided, cord paralysis results. A nonrecurrent laryngeal nerve is most often noted on the right side of the neck.

The CCA is mobilized proximal to the carotid lesion. Dissection is continued upward to isolate the external carotid artery (ECA). The internal carotid artery (ICA) is mobilized up to a point where the vessel is completely normal.

Because the hypoglossal nerve may be injured by retraction, every effort should be made to minimize traction on this nerve. Mobilization of the hypoglossal nerve may require division of the tethering artery and vein to the sternocleidomastoid, the descending hypoglossal branch of the ansa cervicalis, or the occipital artery in order to expose the distal ICA.

Careful attention should also be given to the superior laryngeal nerve, which is usually located medial to the ICA. This nerve divides into external and internal branches that pass posterior to the superior thyroid artery and may be harmed while the surgeon is attempting to control either this vessel or the ICA. The glossopharyngeal nerve crosses the ICA near the base of the skull and is best protected by maintaining dissection close to the anterior surface of the ICA.

Excessive or prolonged retraction of the upper aspect of the incision may cause temporary compression injuries either to the greater auricular nerve laterally or to the marginal mandibular branch of the facial nerve medially.

In patients with a high carotid bifurcation or an extensive lesion, mobilizing the ICA distally can be achieved through several maneuvers, as follows:

  • The skin incision can be extended up to the mastoid process, with complete mobilization of the sternocleidomastoid toward its tendinous insertion on the mastoid process; care must be taken not to injure the accessory nerve, which enters the substance of the sternocleidomastoid at that level
  • The digastric muscle can be mobilized anteriorly or, if necessary, divided
  • If further exposure is needed, the styloid process can be transected, and the mandible can be subluxed anteriorly

Control of the CCA is obtained proximal to the level of disease by surrounding the vessel with an umbilical tape. If sinus bradycardia develops, 1-2 mL of 1% lidocaine is injected into the tissues of the carotid bifurcation to correct reflex sympathetic bradycardia. Once proximal control is obtained, dissection is continued distally around the ECA and its first branch, the superior thyroid artery. Subsequently, control is obtained distally at the ICA.

Throughout the dissection, it is important to minimize manipulation of the carotid artery so as to reduce the risk of embolization. Dissection must be carried out with extreme care not to injure surrounding nerves, most notably the vagus and hypoglossal nerves. The ansa cervicalis, a branch of the hypoglossal nerve, may have to be divided to facilitate the dissection; this is acceptable.

Arteriotomy and shunting

Heparin (5000-7000 U) is administered intravenously (IV). The ICA, the CCA, and the ECA are occluded, in that order. An arteriotomy is made with a No. 11 blade, starting anteriorly on the CCA proximal to the lesion and extending cephalad through the plaque opposite the flow divider, then continued into the ICA with Potts scissors. Distal to the plaque, the arteriotomy is extended until it reaches a point where the ICA is relatively normal.

When general anesthesia is used without cerebral monitoring or when neurologic changes are noted during monitoring, a shunt is placed by inserting the distal end of the shunt into the normal ICA distal to the lesion. Back-bleeding the shunt clears any air or debris, and the proximal end of the shunt is then placed well into the CCA, proximal to the plaque.

Removal of plaque

The endarterectomy proper is begun with a Penfield elevator. The optimal endarterectomy plane is that between the inner and outer medial layers.

The proximal endpoint is obtained by sharply dividing the plaque in the CCA. The plaque can be elevated under full vision while the endarterectomy is continued into the carotid bulb. Carotid plaque that extends a short distance into the ICA may be teased medially toward the origin of the ECA to achieve an adequate endpoint. The plaque can also be divided in the bulb so that the ICA and ECA endarterectomies can be conducted independently.

Once the plaque is divided, the device (clamp or loop) used to control the ECA is loosened, and an eversion endarterectomy is performed. In the ICA, the divided plaque is feathered so that a smooth taper is achieved in the transition to the normal distal intima. If a smooth distal taper is not achieved, placement of interrupted 7-0 monofilament tacking sutures may be necessary to secure the endpoint.

After completion of the endarterectomy, all residual debris and medial fibers are excised because of their potential contribution to embolization or hyperplastic restenosis. The endarterectomy surface is irrigated with heparinized saline solution to facilitate visualization and removal of all debris. Before the clamps are removed, flushing must be done from each direction. The ICA is unclamped last.

Closure

As a rule, a conventional CEA is closed with a patch angioplasty. Although patch angioplasty closure is routine in all patient groups, its benefits are most apparent in women, patients with small ICAs, current smokers, and patients who have previously undergone ipsilateral carotid surgery. Various patch materials have been used with excellent results, including the following:

  • Autogenous saphenous vein
  • Internal jugular vein
  • Polytetrafluoroethylene (PTFE)
  • Dacron
  • Bovine pericardium

Double-armed 6-0 polypropylene sutures are typically used, though when PTFE patches are used, PTFE suture seems to reduce needle-hole bleeding.

Before closure is completed, heparinized saline solution is used to flush the ECA, the ICA, and the CCA. The shunt is removed, and the final few stitches are placed. Flow is then reestablished to the ECA and subsequently to the ICA. Complete hemostasis is obtained. In combined CEA–coronary artery bypass grafting (CABG) procedures, a closed suction drain is placed and is removed the following morning. The wounds are closed with subcuticular stitches.

Postoperative care

Patients are awakened in the operating room, where the surgeon ensures that no neurologic deficit is present. They are then transferred to the recovery room and observed for approximately 6 hours. Postoperative care should include monitoring of the patient’s neurologic status, blood pressure control, and wound observation for hematoma.

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Eversion Endarterectomy

Eversion CEA (eCEA) is an alternative to conventional CEA (see Eversion Carotid Endarterectomy). In an eCEA, preparation and exposure are identical to those in a conventional CEA, except that the carotid bifurcation and the ICA are more completely mobilized.

Instead of being opened with a longitudinal arteriotomy, the ICA is obliquely transected through the bifurcation in such a way as to include a small portion of the CCA. The endarterectomy is started from the cut end of the ICA; the artery is rolled back over the plaque, allowing the diseased intima and media to be removed intact.

The arteriotomy can be extended onto the CCA to allow removal of CCA plaque. The ICA is then anastomosed to the CCA in an end-to-side fashion. If the CCA arteriotomy was extended, a corresponding extension up the ICA will be necessary. Drawing the ICA down to the CCA to create an anastomosis effectively foreshortens the ICA and eliminates redundancy. This technique allows shunt placement, does not require patch angioplasty, and is ideal for patients with ICA redundancy.

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Complications

Hypotension

Carotid baroreceptor stimulation after CEA may cause hypotension. Removal of the carotid plaque causes the carotid bulb to transmit increased arterial pulsation to the carotid sinus nerve, sometimes resulting in reflex bradycardia and hypotension.

Bradycardia during CEA is treated with local infiltration of lidocaine around the nerve and carotid sinus. Blocking the reflex arc by administering atropine sulfate while volume deficits are corrected frequently returns the blood pressure to the normal range. Postoperative pressor support may be necessary; if such support is required, it should last no longer than 6-24 hours in most patients.

Hypertension

Interference with the baroreceptor mechanisms of the carotid sinus may contribute to postoperative blood pressure fluctuation, as may cerebral renin production during carotid clamping and the use of halogenated fluorocarbon general anesthesia.

Adequate preoperative management of patients with hypertension is critical to minimize the deleterious effect on myocardial function and to decrease the incidence of neurologic deficit and hyperperfusion in these patients. Perioperative hypertension should be promptly treated with sodium nitroprusside or other vasoactive agents.

Wound hematoma

The incidence of wound hematomas requiring reoperation is lower than 1%. The use of antiplatelet agents and intraoperative heparin anticoagulation contribute to this bleeding risk. However, these agents are required to reduce the risk of coronary or cerebrovascular thrombotic events. A large cervical hematoma may compress the ICA and adjacent cranial nerves; it also may compromise the airway and be a potential nidus of infection. Significant perioperative hematomas should be surgically drained.

Infection and false aneurysm

Wound infection after CEA is extremely rare. Infected false aneurysms occur at a rate of only 0.15%. Infected false aneurysms should be treated with excision of all infected vascular tissues and surrounding soft tissue infection. Ideally, the carotid circulation should be reestablished with an interposition vein graft.

When the carotid bifurcation is excised, the authors usually make no effort to reconstruct the ECA. In cases where reconstruction may be technically challenging (eg, prior neck irradiation or extensive infection), ligation and resection without reconstruction may be necessary. In such cases, the authors perform preoperative angiography with test balloon occlusion of the ICA with the patient awake to obtain information on the potential consequences of carotid ligation.

Cranial nerve dysfunction

The reported incidence of cranial nerve injury after CEA ranges from a few percent up to 39%. Approximately 60% of these injuries are symptomatic, mostly related to superior laryngeal and recurrent laryngeal nerve dysfunction. Hoarseness is the most common finding; fortunately, it is temporary in most cases.

Injury to vagus nerve and branches (recurrent and superior laryngeal nerves)

Injury to the vagus nerve or the recurrent laryngeal nerve can be caused by retractors or by direct trauma from the use of forceps, electrocauterization, or the application of arterial clamps. Paralysis of the ipsilateral vocal cord usually results in hoarseness and loss of an effective cough mechanism. Unilateral injury to the vagus nerve or recurrent laryngeal nerve can be asymptomatic but becomes significant when bilateral carotid reconstruction is planned.

Routine laryngoscopic visualization of the vocal cords is recommended when staged bilateral CEA is planned. The superior laryngeal nerve is responsible for the quality of the voice, especially higher pitches.

Injury to hypoglossal nerve

Mobilization of the hypoglossal nerve is commonly necessary, especially when a high carotid bifurcation is present. Division of small veins that tent the nerve downward, along with the branches of the ECA to the sternocleidomastoid, facilitates mobilization, as does division of the ansa cervicalis as it comes off the hypoglossal nerve. Injury to this nerve is manifested by deviation of the tongue to the ipsilateral side; on occasion, however, a mastication problem, deglutition, or speech impairment may be noted.

Injury to glossopharyngeal nerve

In a normal CEA dissection, the glossopharyngeal nerve usually is not seen; however, it can be injured when the dissection is continued upward because of a high carotid bifurcation or a high ICA lesion. This nerve can be injured with improper clamping, during division of the digastric muscle, or by mandibular subluxation and detachment of the styloid process during high carotid dissection. Injury causes paralysis of the middle pharyngeal constrictor muscle, and this may cause difficulty in swallowing solid foods.

Horner syndrome

Horner syndrome may be produced by injury to the ascending sympathetic fibers in the area of the glossopharyngeal nerve.

Injury to facial nerve branch

The marginal mandibular branch of the facial nerve can be injured when the incision is close to the jaw; more commonly, it may be injured by upward pressure of a retractor against the mandible. Trauma to this nerve causes sagging of the ipsilateral corner of the mouth. Injury can be prevented by curving the upper portion of the incision toward the mastoid process and by using retractors carefully, with intermittent release of tension.

Hyperperfusion and cerebral hemorrhage

The classic presentation of hyperperfusion and cerebral hemorrhage syndrome is unilateral headache, seizure, and cerebral hemorrhage, peaking at postoperative days 2-7. The incidence of hyperperfusion is 2-3%, which progresses to cerebral hemorrhage in 0.2-0.8% of cases.[13] This serious complication can be minimized by good preoperative blood pressure control and staged treatment of severe bilateral stenosis.

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Contributor Information and Disclosures
Author

Omar Haqqani, MD MidMichigan Health

Omar Haqqani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Medical Association, New York Academy of Sciences, Sigma Xi, Society for Vascular Surgery, American Society of Clinical Oncology, American Federation for Clinical Research, American Venous Forum, Vascular and Endovascular Surgery Society, Eastern Vascular Society, Society for Clinical Vascular Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

Mark David Iafrati, MD RVT, FACS, Chief of Vascular Surgery, Director Center for Wound Healing, The Cardiovascular Center, Tufts Medical Center; Assistant Professor of Surgery, Tufts University School of Medicine; Assistant Professor of Surgery, Uniformed Services University of the Health Sciences

Mark David Iafrati, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association of Military Surgeons of the US, Massachusetts Medical Society, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Critical Care Medicine, Society of Laparoendoscopic Surgeons, American Venous Forum, Society for Clinical Vascular Surgery

Disclosure: Nothing to disclose.

James M Estes, MD Assistant Professor of Surgery, Tufts University School of Medicine; Medical Director of Vascular Laboratory, Attending Surgeon, Tufts Medical Center; Attending Surgeon, Morton Hospital

James M Estes, MD is a member of the following medical societies: American College of Surgeons, Association for Surgical Education, Society for Vascular Surgery, Eastern Vascular Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

References
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  3. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1991 Aug 15. 325(7):445-53. [Medline].

  4. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995 May 10. 273(18):1421-8. [Medline].

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  7. Landis GS, Faries PL. A critical look at "high-risk" in choosing the proper intervention for patients with carotid bifurcation disease. Semin Vasc Surg. 2007. 20:199-204.

  8. Schechter MA, Shortell CK, Scarborough JE. Regional versus general anesthesia for carotid endarterectomy: the American College of Surgeons National Surgical Quality Improvement Program perspective. Surgery. 2012 Sep. 152(3):309-14. [Medline].

  9. Ricotta JJ, DeWeese JA. Is routine carotid ultrasound surveillance after carotid endarterectomy worthwhile?. Am J Surg. 1996 Aug. 172(2):140-2; discussion 143. [Medline].

  10. Lal BK, Beach KW, Roubin GS, Lutsep HL, Moore WS, Malas MB, et al. Restenosis after carotid artery stenting and endarterectomy: a secondary analysis of CREST, a randomised controlled trial. Lancet Neurol. 2012 Sep. 11(9):755-63. [Medline].

  11. Geraghty PJ, Brothers TE, Gillespie DL, Upchurch GR, Stoner MC, Siami FS, et al. Preoperative symptom type influences the 30-day perioperative outcomes of carotid endarterectomy and carotid stenting in the Society for Vascular Surgery Vascular Registry. J Vasc Surg. 2014 Sep. 60(3):639-44. [Medline].

  12. Bonati LH, Dobson J, Featherstone RL, Ederle J, van der Worp HB, de Borst GJ, et al. Long-term outcomes after stenting versus endarterectomy for treatment of symptomatic carotid stenosis: the International Carotid Stenting Study (ICSS) randomised trial. Lancet. 2014 Oct 14. [Medline].

  13. Ascher E, Markevich N, Schutzer RW, Kallakuri S, Jacob T, Hingorani AP. Cerebral hyperperfusion syndrome after carotid endarterectomy: predictive factors and hemodynamic changes. J Vasc Surg. 2003 Apr. 37(4):769-77. [Medline].

 
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Carotid endarterectomy: operative techniques.
Anatomy of internal carotid and vertebral arteries.
 
 
 
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