Management of the Neck With Carotid Artery Involvement

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Management of the Neck With Carotid Artery Involvement

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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.

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. [13] However, its use as definitive therapy in patients with long-term survival potential is discouraged. [14, 15] 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. [16] 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 [17]

20

7

0

7

3

4

2

Konno et al [16]

156

53

6

47

24

. . .

. . .

Razack and Sako [18]

77

25

1

24

4

. . .

. . .

 

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. [19] 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. [20] 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. [21] 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.

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.

Wright JG, Nicholson R, Schuller DE, Smead WL. Resection of the internal carotid artery and replacement with greater saphenous vein: a safe procedure for en bloc cancer resections with carotid involvement. J Vasc Surg. 1996 May. 23(5):775-80; discussion 781-2. [Medline].

Freeman SB, Hamaker RC, Borrowdale RB, Huntley TC. Management of neck metastasis with carotid artery involvement. Laryngoscope. 2004 Jan. 114(1):20-4. [Medline].

Huvos AG, Leaming RH, Moore OS. Clinicopathologic study of the resected carotid artery. Analysis of sixty-four cases. Am J Surg. 1973 Oct. 126(4):570-4. [Medline].

McCready RA, Miller SK, Hamaker RC, Singer MI, Herod GT. What is the role of carotid arterial resection in the management of advanced cervical cancer?. J Vasc Surg. 1989 Sep. 10(3):274-80. [Medline].

Ozer E, Agrawal A, Ozer HG, Schuller DE. The impact of surgery in the management of the head and neck carcinoma involving the carotid artery. Laryngoscope. 2008 Oct. 118(10):1771-4. [Medline].

Roh JL, Kim MR, Choi SH, et al. Can patients with head and neck cancers invading carotid artery gain survival benefit from surgery?. Acta Otolaryngol. 2008. 128(12):1370-4. [Medline].

Manzoor NF, Russell JO, Bricker A, Koyfman S, Scharpf J, Burkey B, et al. Impact of surgical resection on survival in patients with advanced head and neck cancer involving the carotid artery. JAMA Otolaryngol Head Neck Surg. 2013 Nov. 139(11):1219-25. [Medline].

Sanna M, Piazza P, Ditrapani G, Agarwal M. Management of the internal carotid artery in tumors of the lateral skull base: preoperative permanent balloon occlusion without reconstruction. Otol Neurotol. 2004 Nov. 25(6):998-1005. [Medline].

Kalani MY, Kalb S, Martirosyan NL, Lettieri SC, Spetzler RF, Porter RW, et al. Cerebral revascularization and carotid artery resection at the skull base for treatment of advanced head and neck malignancies. J Neurosurg. 2013 Mar. 118(3):637-42. [Medline].

Yoo GH, Hocwald E, Korkmaz H, et al. Assessment of carotid artery invasion in patients with head and neck cancer. Laryngoscope. 2000 Mar. 110(3 Pt 1):386-90. [Medline].

Yousem DM, Hatabu H, Hurst RW, et al. Carotid artery invasion by head and neck masses: prediction with MR imaging. Radiology. 1995 Jun. 195(3):715-20. [Medline].

Pons Y, Ukkola-Pons E, Clément P, Gauthier J, Conessa C. Relevance of 5 different imaging signs in the evaluation of carotid artery invasion by cervical lymphadenopathy in head and neck squamous cell carcinoma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010 May. 109(5):775-8. [Medline].

Bond KM, Brinjikji W, Murad MH, Cloft HJ, Lanzino G. Endovascular treatment of carotid blowout syndrome. J Vasc Surg. 2017 Mar. 65 (3):883-8. [Medline].

Wan WS, Lai V, Lau HY, Wong YC, Poon WL, Tan CB. Endovascular treatment paradigm of carotid blowout syndrome: review of 8-years experience. Eur J Radiol. 2013 Jan. 82(1):95-9. [Medline].

Liang NL, Guedes BD, Duvvuri U, et al. Outcomes of interventions for carotid blowout syndrome in patients with head and neck cancer. J Vasc Surg. 2016 Jun. 63 (6):1525-30. [Medline].

Konno A, Togawa K, Iizuka K. Analysis of factors affecting complications of carotid ligation. Ann Otol Rhinol Laryngol. 1981 May-Jun. 90(3 Pt 1):222-6. [Medline].

Maves MD, Bruns MD, Keenan MJ. Carotid artery resection for head and neck cancer. Ann Otol Rhinol Laryngol. 1992 Sep. 101(9):778-81. [Medline].

Razack MS, Sako K. Carotid artery hemorrhage and ligation in head and neck cancer. J Surg Oncol. 1982 Apr. 19(4):189-92. [Medline].

Jones TH, Morawetz RB, Crowell RM, et al. Thresholds of focal cerebral ischemia in awake monkeys. J Neurosurg. 1981 Jun. 54(6):773-82. [Medline].

Ehrnefeld WK, Stoney RJ, Wylie EJ. Relation of carotid stump pressure to safety of carotid artery ligation. Surgery. 1983 Feb. 93(2):299-305. [Medline].

Kelly JJ, Callow AD, O’Donnell TF, et al. Failure of carotid stump pressures. Its incidence as a predictor for a temporary shunt during carotid endarterectomy. Arch Surg. 1979 Dec. 114(12):1361-6. [Medline].

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Standard SC, Ahuja A, Guterman LR, et al. Balloon test occlusion of the internal carotid artery with hypotensive challenge. AJNR Am J Neuroradiol. 1995 Aug. 16(7):1453-8. [Medline].

Andersen AR, Friberg HH, Schmidt JF, Hasselbalch SG. Quantitative measurements of cerebral blood flow using SPECT and [99mTc]-d,l-HM-PAO compared to xenon-133. J Cereb Blood Flow Metab. 1988 Dec. 8(6):S69-81. [Medline].

Erba SM, Horton JA, Latchaw RE, et al. Balloon test occlusion of the internal carotid artery with stable xenon/CT cerebral blood flow imaging. AJNR Am J Neuroradiol. 1988 May-Jun. 9(3):533-8. [Medline].

Witt JP, Yonas H, Jungreis C. Cerebral blood flow response pattern during balloon test occlusion of the internal carotid artery. AJNR Am J Neuroradiol. 1994 May. 15(5):847-56. [Medline].

Adams GL, Madison M, Remley K, Gapany M. Preoperative permanent balloon occlusion of internal carotid artery in patients with advanced head and neck squamous cell carcinoma. Laryngoscope. 1999 Mar. 109(3):460-6. [Medline].

Eckard DA, Purdy PD, Bonte FJ. Temporary balloon occlusion of the carotid artery combined with brain blood flow imaging as a test to predict tolerance prior to permanent carotid sacrifice. AJNR Am J Neuroradiol. 1992 Nov-Dec. 13(6):1565-9. [Medline].

Gonzalez CF, Moret J. Balloon occlusion of the carotid artery prior to surgery for neck tumors. AJNR Am J Neuroradiol. 1990 Jul-Aug. 11(4):649-52. [Medline].

Meleca RJ, Marks SC. Carotid artery resection for cancer of the head and neck. Arch Otolaryngol Head Neck Surg. 1994 Sep. 120(9):974-8. [Medline].

de Vries EJ, Sekhar LN, Horton JA, et al. A new method to predict safe resection of the internal carotid artery. Laryngoscope. 1990 Jan. 100(1):85-8. [Medline].

Segal DH, Sen C, Bederson JB, Catalano P, Sacher M, Stollman AL. Predictive value of balloon test occlusion of the internal carotid artery. Skull Base Surg. 1995. 5(2):97-107. [Medline].

Nishioka H. Results of the treatment of intracranial aneurysms by occlusion of the carotid artery in the neck. J Neurosurg. 1966 Dec. 25(6):660-704. [Medline].

Youmans JR, Kindt GW, Mitchell OC. Extended studies of direction of flow and pressure in the internal carotid artery following common carotid artery ligation. J Neurosurg. 1967 Sep. 27(3):250-4. [Medline].

Kroeker TR, O’Brien JC. Carotid resection and reconstruction associated with treatment of head and neck cancer. Proc (Bayl Univ Med Cent). 2011 Oct. 24(4):295-8. [Medline]. [Full Text].

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Barnett HJ. Delayed cerebral ischemic episodes distal to occlusion of major cerebral arteries. Neurology. 1978 Aug. 28(8):769-74. [Medline].

Teymoortash A, Rassow S, Bohne F, Wilhelm T, Hoch S. Clinical impact of radiographic carotid artery involvement in neck metastases from head and neck cancer. Int J Oral Maxillofac Surg. 2016 Apr. 45 (4):422-6. [Medline].

Chung EJ, Kwon KH, Yoon DY, Cho SW, Kim EJ, Rho YS. Clinical outcome analysis of 47 patients with advanced head and neck cancer with preoperative suspicion of carotid artery invasion. Head Neck. 2016 Apr. 38 Suppl 1:E287-92. [Medline].

Berenstein A, Ransohoff J, Kupersmith M, Flamm E, Graeb D. Transvascular treatment of giant aneurysms of the cavernous carotid and vertebral arteries. Functional investigation and embolization. Surg Neurol. 1984 Jan. 21(1):3-12. [Medline].

Freeman SB, Hamaker RC, Borrowdale RB, Huntley TC. Management of neck metastasis with carotid artery involvement. Laryngoscope. 2004 Jan. 114(1):20-4. [Medline].

German WJ, Black SP. Cervical ligation for internal carotid aneurysms. An extended follow-up. J Neurosurg. 1965 Dec. 23(6):572-7. [Medline].

Wright JG, Nicholson R, Schuller DE, Smead WL. Resection of the internal carotid artery and replacement with greater saphenous vein: a safe procedure for en bloc cancer resections with carotid involvement. J Vasc Surg. 1996 May. 23(5):775-80; discussion 781-2. [Medline].

Study

Number of Patients

Number of Events

Temporary Ischemia

Permanent Cerebral Vascular Accident (CVA)

Deaths CNS

Total Deaths

Embolic Blindness

Maves et al [17]

20

7

0

7

3

4

2

Konno et al [16]

156

53

6

47

24

. . .

. . .

Razack and Sako [18]

77

25

1

24

4

. . .

. . .

Devraj Basu, MD, PhD, FACS Assistant Professor, Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania Health System

Devraj Basu, MD, PhD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Association for Cancer Research, American College of Surgeons, American Head and Neck Society

Disclosure: Nothing to disclose.

John M Truelson, MD, FACS Chairman, Division of Head and Neck Surgery, Associate Professor, Department of Otorhinolaryngology, University of Texas Southwestern Medical Center at Dallas

John M Truelson, MD, FACS is a member of the following medical societies: American Head and Neck Society, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, Phi Beta Kappa, Texas Medical Association

Disclosure: Nothing to disclose.

Gregory S Weinstein, MD, FACS Professor and Vice-Chairman, Department of Otorhinolaryngology-Head and Neck Surgery, Director of Division of Head and Neck Surgery, Director of Head and Oncology Fellowship, Director of Otorhinolaryngology-Head and Neck Clinic, Co-director of The Center for Head and Neck Surgery, University of Pennsylvania School of Medicine

Gregory S Weinstein, MD, FACS is a member of the following medical societies: American Head and Neck Society, American Laryngological Association, American Radium Society, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of University Otolaryngologists-Head and Neck Surgeons, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, The Triological Society, American Medical Association

Disclosure: Nothing to disclose.

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.

Nader Sadeghi, MD, FRCSC Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, McGill University Faculty of Medicine; Chief Otolaryngologist, MUHC; Director, McGill Head and Neck Cancer Program, Royal Victoria Hospital, Canada

Nader Sadeghi, MD, FRCSC is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society, American Thyroid Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.

Richard V Smith, MD Director of Clinical Affairs, Associate Professor, Department of Otolaryngology, Division of Head and Neck Surgery, Einstein College of Medicine, Montefiore Medical Center

Richard V Smith, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Head and Neck Society, The Triological Society, American Medical Association, American Medical Student Association/Foundation, Medical Society of the District of Columbia, New York Academy of Medicine, Vermont Medical Society

Disclosure: Nothing to disclose.

Management of the Neck With Carotid Artery Involvement

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Management of the Neck With Carotid Artery Involvement

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