Management of the Neck With Carotid Artery Involvement

Updated: Mar 19, 2014
  • Author: Devraj Basu, MD, PhD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
  • Print
Overview

Background

Malignant invasion of the carotid artery presents the head and neck oncologist with both diagnostic and therapeutic challenges. When resection of the carotid artery as part of a cancer surgery is considered, preoperative evaluation can identify which patients are at greatest risk of neurologic sequelae, and carotid reconstruction must be considered whenever possible to decrease the risk of such complications. [1] Unfortunately, even with reconstruction, patients still bear some risk of immediate and delayed neurologic sequelae from the procedure. Furthermore, long-term survival is generally poor in cases of malignant carotid involvement, even when the surgical resection of the carotid proceeds uneventfully.

In modern head and neck oncologic practice, high radiologic suspicion of carotid invasion is considered by some to be a contraindication to primary surgical therapy because of the risk of stroke with carotid resection. [2] As a result, many individuals in whom carotid resection is considered have previously been treated with radiotherapy and have persistent or recurrent malignancy in an irradiated field.

Attempting surgical salvage in this population presents additional challenges. First, carotid invasion is more difficult to predict based on preoperative CT imaging or MRI in this population. Thus, the surgeon must entertain the possibility of invasion even in the absence of bulky disease or carotid encasement. At the same time, the radiographic or intraoperative appearance of carotid involvement can merely represent inflammatory changes and fibrosis in an irradiated field, mimicking invasion when none is present.

This unpredictability is highlighted by multiple pathologic series in which only a minority (37.5-42%) of resected carotid arteries are shown histologically to be invaded. [3, 4] Secondly, irradiated patients have arterial walls that are weakened because of adventitial fibrosis, destruction of the arterial elastic tissue, and accelerated atherosclerosis. Aggressive subadventitial dissection in this case can lead to either intraoperative rupture or high risk of postoperative rupture if wound complications prevent adequate protection of the vessel.

Next:

Indications

Carotid ligation/resection/endovascular stenting

Carotid wall invasion most often arises either from direct extension of a primary head and neck squamous cell carcinoma of the pharynx or from bulky jugular chain lymph node metastasis with extracapsular extension. Although labeled "unresectable" by current AJCC staging criteria, such individuals may be selectively considered for carotid resection as part of primary surgical therapy or a salvage attempt after prior radiotherapy and chemotherapy.

Some recent case series do advocate selective use of carotid resection as part of primary surgical therapy for head and neck carcinomas. [5, 6, 7] These studies suggest better disease-free survival from carotid resection than with nonsurgical therapy for previously untreated patients. This result is not surprising, as primary surgical resection remains the preferred mode of therapy, when deemed feasible, for the types of massive volume tumors that typically lead to carotid invasion. A further rationale for surgery in these untreated patients is that a high proportion of tumors suggested to invade the carotid wall radiographically can ultimately be removed without carotid resection.

Occasionally, benign tumors of the lateral skull base, such as glomus jugulare tumors and schwannomas, as well as various skull base malignancies, may necessitate planned carotid resection. [8] Resection of the internal carotid artery for malignant disease at its entry into the carotid canal can be reconstructed using intracranial bypass but has not been advocated because of unfavorable outcomes. [9]

Clinically, carotid invasion is suggested when a tumor abutting the carotid sheath feels fixed or hypomobile, particularly in the vertical dimension. In the previously untreated neck, carotid arteries that are abutted less than 180o of their circumference by imaging are highly unlikely to require carotid resection. For arteries with greater than 180o of tumor abutment, obliteration of tissue planes between the artery and the tumor on MRI suggests invasion but can be difficult to interpret, particularly in the postradiation salvage setting.

Importantly, involvement of greater than 180° of the carotid circumference is not clearly predictive of histologic invasion, [10] with clinical assessment being of at least equal value. Involvement of the artery 270o or more does accurately predict the surgeon's inability to remove tumor from the artery wall. [11]

In addition, compressive deformity of the artery wall by a closely abutting tumor appears also highly predictive of carotid invasion. [12] In cases in which carotid involvement is feasible based on clinical and radiographic criteria, pursuing surgery requires additional preoperative planning, including involvement of a vascular surgeon in cases in which artery reconstruction is feasible, as well as consideration of angiography with balloon-occlusion testing.

Occasionally, in cases of carotid blowout, emergent carotid ligation and/or resection may be needed without any preoperative testing. In this scenario, reconstruction is still favorable whenever possible, although it may be impractical in a surgical field containing an uncontrolled fistula, which may have caused the rupture itself. Impending rupture is often signaled by minor sentinel bleeding, which can be controlled initially with conservative measures, allowing time for assessment with angiography and consideration of neurointerventional versus open surgical approaches.

In the setting of blowout or sentinel bleed, endovascular stenting may be a useful temporizing or palliative care measure if emergent neurointerventional radiology services are available. However, its use as definitive therapy in patients with long-term survival potential is discouraged. [13] Problems include need for subsequent anticoagulation in a high bleeding-risk setting and intractable bacterial colonization of the stent associated with placement in an infected, radiated wound.

The 3 studies in the table below demonstrate the high morbidity and mortality associated with carotid ligation without reconstruction or preoperative testing. In the largest series, no difference was noted in complications associated with the reason for ligation, which included cancer infiltration, impending rupture, and acute rupture. [14] The incidence of cerebral complications significantly decreased in patients whose common carotids were occluded gradually over 8 days or longer (5.3%), compared with patients with ligation for less than 7 days (30.6%) or those patients with abrupt ligation (42%).

Table. Morbidity and Mortality Associated With Carotid Ligation Without Reconstruction or Preoperative Testing (Open Table in a new window)

Study Number of Patients Number of Events Temporary Ischemia Permanent Cerebral Vascular Accident (CVA) Deaths CNS Total Deaths Embolic Blindness
Maves et al [15] 20 7 0 7 3 4 2
Konno et al [14] 156 53 6 47 24 . . . . . .
Razack and Sako [16] 77 25 1 24 4 . . . . . .

 

Previous
Next:

Relevant Anatomy

The physiology of carotid flow

Preoperative testing and perioperative management of hemodynamics after carotid resection are based on an understanding of cerebral blood flow (CBF) regulation. Under normal physiologic conditions, the average CBF is 50-55 mm/100 g/min, a range that is maintained by the autoregulation capacity of cerebral vasculature. However, in significant hypotension, autoregulation is lost and the CBF fluctuates with arterial blood pressure. Generally, CBF must decrease to 20-25 mL/100 g/min for brain dysfunction to occur. Management of systemic blood pressure can thus be critical for maintaining cerebral perfusion in individuals having undergone carotid resection, even in the absence of immediate posttreatment neurologic sequelae. Delayed onset symptoms and even a cerebral vascular accident (CVA) may develop in patients after carotid occlusion if systemic blood pressure drops.

The timing of permanent brain injury from ischemia has been well characterized in a primate model. [17] Here, the neurologic symptoms that result from obstruction of the middle cerebral artery were partially reversible for up to 3 hours after occlusion. Microscopic infarcts were observed after 15-30 minutes and moderate-to-large infarction 2-3 hours later. After 3 hours, large permanent infarcts developed. With a regional CBF of less than 23 mL/100 g/min, reversible paralysis occurred. With a regional CBF of less than 10-12 mL/100 g/min for 2-3 hours or of less than 17-18 mL/100 g/min during permanent occlusion, the animals developed irreversible neurologic sequelae.

Stump pressure is an important concept for intraoperative decision making in managing cases of sudden rupture or unexpected carotid involvement. [18] Brisk backflow from the distal carotid stump is a reflection of stump pressure, which is regarded as an indicator of adequate collateral blood flow when the carotid is occluded proximally. Though rarely used clinically, this value may be measured with a strain gauge attached to a 19-gauge needle in the experimental setting. Although stump pressures of more than 50-70 mm Hg are considered low risk, caution is still warranted because intraoperative electroencephalogram changes have been demonstrated at higher pressures. [19] In general, the common carotid artery produces higher stump pressures than the internal carotid artery, if the external carotid artery system is intact and thus available to provide backflow. This difference accounts for the significantly higher risks associated with ligation of the internal versus common carotid artery.

Previous
Next:

Contraindications

Contraindications to surgical management of the neck with carotid artery involvement are based on the patient's comorbidities and ability to tolerate surgery, as well as the technical feasibility of extirpating the tumor. Although few absolute contraindications exist, decision making is heavily influenced by the patient's overall functional status, the anticipated natural course of the tumor, consideration of nonsurgical options, and the patient's level of enthusiasm for surgery given the risk of severe neurologic sequelae or even death.

Previous