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Lymph node compression causes stenotic kinking of the internal carotid artery
Case Report
Lymph Node Compression Causes Stenotic Kinking of the Internal Carotid Artery Kyo Niijima,
MD, PhD
A 34-year-old woman presented with recurrent transient ischemic attack (TIA) of the left hemiparesis. Carotid angiography disclosed a stenotic kinking of the right internal carotid artery (ICA). The patient underwent exploration of the right ICA for a planned endarterectomy. An enlarged lymph node was found to have compressed and kinked the artery. The lymph node was removed, and segmental resection of the kinked, stenosed, and atrophic ICA, followed by end-to-end reanastomosis, was performed with successful result. Histologically, the lymph node was calcified, and the atrophy of the ICA, the lumen of which was smooth without atheroma, was localized at the site of compression. Based on the findings of the stenotic kinking of the ICA, long-standing compression by the lymph node was the most probable cause of the kinking, rather than the atherosclerotic change of the ICA. Key Words: Kinking—Internal carotid artery—Transient ischemic attack—Lymph node.
A transient ischemic attack (TIA) caused by atherosclerotic stenosis of the internal carotid artery (ICA) just distal to the carotid bifurcation is common. This pathology has been universally and successfully treated by carotid endarterectomy for decades.1,2 Surgical treatment to prevent disabling stroke is also indicated for a stenotic kinking of the ICA, with or without atherosclerosis, presenting cerebral ischemia.3 I recently experienced a case of TIA caused by stenotic kinking of the ICA. At the time of surgery, the ICA was found to be compressed by an enlarged lymph node.
From the Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY. Received December 1, 1999; accepted February 4, 2000. Address reprint requests to Kyo Niijima, MD, PhD, 5-22-7 Kitakutsukake-cho, Oe, Nishikyo-ku, Kyoto 610-1101, Japan. Copyright © 2000 by National Stroke Association 1052-3057/00/0905-0007$3.00/0 doi:10.1053/jscd.2000.9886
250
Case Report A 34-year-old woman had experienced recurrent attacks of left motor hemiparesis for 2 years. The attacks were occasionally evoked by rotation of the patient’s neck to the right. None of her family members has suffered from cerebrovascular and/or coronary disease. This nonsmoking patient, who was not diabetic, hypertensive or hyperlipidemic, showed no neurologic deficit at the time of admission. Inspection of her head and neck uncovered no abnormality, and cervical bruit was not audible. Neither leukocytosis nor abnormally high C-reactive protein was seen in the laboratory data. Platelet aggregation had been controlled to between 33% and 48% for 18 months after administration of 200 mg/day of ticlopidine hydrochloride had been begun. The results of both electro- and echocardiogram were within normal limits. Chest radiographs showed no lesion or abnormal calcification. Magnetic resonance imaging (MRI) of the brain showed lacunar infarctions of the bilateral basal ganglia. Hypoperfusion of the frontotemporal region on the right side was demonstrated by cerebral blood flow (CBF) measurements by using technetium Tc99m hexyl-
Journal of Stroke and Cerebrovascular Diseases, Vol. 9, No. 5 (September-October), 2000: pp 250-253
ICA KINKING BY LYMPH NODE
methyl propylene amineoxine single photon emission computed tomography (99mTcHMPAO SPECT). No microemboli were detected by Doppler sonography. The right common carotid angiography disclosed a stenotic kinking of the ICA, which appeared redundant, about 15 mm distal to the carotid bifurcation (Fig 1). Cross circulation from the left carotid and vertebrobasilar systems through the anterior communicating artery and the right posterior communicating artery was seen. The patient had been asymptomatic for 20 minutes during balloon test occlusion of the right ICA. Because of these findings, a preoperative diagnosis of TIA due to stenotic kinking of the ICA caused by atherosclerosis was made, and the oral antiplatelet agent was continued.
251
The patient underwent exploration of the right ICA for a planned endarterectomy, when an enlarged firm lymph node (⬃15 mm in diameter) was found to have compressed and encroached the artery (Fig 2A). The vessel was tethered caudally and kinked by the lymph node; this was the finding that appeared on the angiogram as a redundancy. Dissection and removal of that lymph node, which adhered to the adventitia of the ICA and the surrounding tissue, was performed, resulting in only about a 10% increase of that carotid blood flow, as detected by intraoperative Doppler study. An arteriotomy showed that the lumen of that segment of the ICA, about 6 mm long, was grossly smooth and narrowed. Because atheromatous plaque was not found and the apparently indented ICA was already atrophic at the compressed part, an endarterectomy was not indicated. Instead, segmental resection (⬃10 mm) of the kinked, stenosed, and atrophic ICA followed by end-to-end reanastomosis was performed by microsurgery (Fig 2B). Pathological examination showed that the lymph node was inactive and calcified and was presumably the result of a previous inflammation. No neoplasm cells were found. The lumen of the resected segment of the ICA was narrowed, and atheromatous change was not evident. The atrophy of the vascular wall was localized around the compressed site. Vasculitis or fibromuscular dysplasia was not seen. The patient has continued to be asymptomatic for 3 years after the surgery. The oral antiplatelet agent had been stopped postoperatively. In the angiography performed 6 months after surgery, the anastomotic site of the ICA was confirmed to be widely patent and normally shaped (Fig 3). Postoperative CBF measurements showed that hypoperfusion of the right frontotemporal area disappeared.
Discussion
Figure 1. Preoperative angiogram of the right common carotid artery showing a stenotic kinking of the ICA, which appears redundant, about 15 mm distal to the carotid bifurcation.
The incidence of tortuousity, coiling, or kinking of the ICA has been estimated at 16% in a series of 1000 angiograms by Metz et al.4 It is reported that 4% to 16% of kinking of the ICA has stenosis.5 Cioffi et al6 found kinking of the ICA in 10.1% of 1010 unselected angiograms, whereas Najafi et al.7 reported a 5% incidence of this lesion in a series of 308 patients who underwent carotid surgery. There were 15 instances of kinking (4.8%) in the series of 312 carotid reconstructions performed by Vannix et al.3 A TIA caused by stenotic kinking of the ICA is not rare.3,8 According to Vannix et al.,3 kinking of the ICA is almost always accompanied by atherosclerosis, which may cause not only a hemodynamic ischemia, but also an embolic one. Although the stenosis of the ICA in this patient was less than 50% according to the North American Symptom-
252
K. NIIJIMA
Figure 2. Intraoperative microphotographs. (A) The kinking (arrow) and tethering of the ICA resulted from compression by the lymph node (LN), which has already been dissected. (B) Segmental resection and end-to-end reanastomosis of the ICA.
atic Carotid Endarterectomy Trial (NASCET) criteria,2 it was most probably responsible for the patient’s cerebrovascular events, based on the surgical outcome. A kinking of the ICA caused by compression by nonvascular masses, such as a parathyroid cyst, brachial cleft cyst, lipoma, cystic hygroma, neoplasm, substernal thyroid, thyroid adenoma, or an enlarged lymph node, was postulated,9 but has not been documented or reviewed in detail. Neurosurgeons and vascular surgeons may not infrequently encounter an enlarged lymph node during
dissection of the cervical ICA for carotid endarterectomy. To my knowledge, however, stenotic kinking of the ICA due to compression by a lymph node has never been reported. In the present case, both macro- and microscopic findings of the stenotic kinking in question suggest that long-standing extraluminal pressure by the calcified lymph node, rather than sclerotic redundancy, was the primary problem. It has been generally accepted that surgical interventions should be indicated in a stenotic kinking of
ICA KINKING BY LYMPH NODE
253
anastomosis of the ICA was considered to be the treatment of choice in this particular case.
References
Figure 3. Postoperative angiogram showing the patent ICA in normal shape.
the ICA, if the lesion is responsible for cerebrovascular insufficiency.7 It is important to presume an unusual cause of stenosis of the ICA when an atypical patient of TIA is encountered and a carotid surgery other than endarterectomy may possibly be worthwhile. Removal of the encroached calcified lymph node followed by resection of the atrophic segment and end-to-end re-
1. European Carotid Surgery Trialists’ Collaborative Group: MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet 1991;337:1235-1243. 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators: Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445-453. 3. Vannix RS, Joergenson EJ, Carter R: Kinking of the internal carotid artery: Clinical significance and surgical management. Am J Surg 1977;134:82-89. 4. Metz H, Murray-Leslie RM, Bannister RG, et al: Kinking of the internal carotid artery in relation to cerebrovascular disease. Lancet 1961;1:424. 5. Koskas F, Bahnini A, Walden R, et al: Stenotic coiling and kinking of the internal carotid artery. Ann Vasc Surg 1993;7:530-540. 6. Cioffi FA, Meduri M, Tomasello F, et al: Kinking and coiling of the internal carotid artery: Clinical statistical observations and surgical perspectives. J Neurosurg Sci 1975;19:15. 7. Najafi H, Javid H, Dye WS, et al: Kinked internal carotid artery. Arch Surg 1964;89:134. 8. Santon PE, McClusky DA Jr, Lamis PA: Hemodynamic assessment and surgical correction of kinking of the internal carotid artery. Surgery 1978;84:793-802. 9. Leipzig TJ, Dormann GJ: The tortuous or kinked carotid artery: Pathogenesis and clinical considerations: A historical review. Surg Neurol 1986;25:478-486.
Lymph Node Compression Causes Stenotic Kinking of the Internal Carotid Artery Kyo Niijima,
MD, PhD
A 34-year-old woman presented with recurrent transient ischemic attack (TIA) of the left hemiparesis. Carotid angiography disclosed a stenotic kinking of the right internal carotid artery (ICA). The patient underwent exploration of the right ICA for a planned endarterectomy. An enlarged lymph node was found to have compressed and kinked the artery. The lymph node was removed, and segmental resection of the kinked, stenosed, and atrophic ICA, followed by end-to-end reanastomosis, was performed with successful result. Histologically, the lymph node was calcified, and the atrophy of the ICA, the lumen of which was smooth without atheroma, was localized at the site of compression. Based on the findings of the stenotic kinking of the ICA, long-standing compression by the lymph node was the most probable cause of the kinking, rather than the atherosclerotic change of the ICA. Key Words: Kinking—Internal carotid artery—Transient ischemic attack—Lymph node.
A transient ischemic attack (TIA) caused by atherosclerotic stenosis of the internal carotid artery (ICA) just distal to the carotid bifurcation is common. This pathology has been universally and successfully treated by carotid endarterectomy for decades.1,2 Surgical treatment to prevent disabling stroke is also indicated for a stenotic kinking of the ICA, with or without atherosclerosis, presenting cerebral ischemia.3 I recently experienced a case of TIA caused by stenotic kinking of the ICA. At the time of surgery, the ICA was found to be compressed by an enlarged lymph node.
From the Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY. Received December 1, 1999; accepted February 4, 2000. Address reprint requests to Kyo Niijima, MD, PhD, 5-22-7 Kitakutsukake-cho, Oe, Nishikyo-ku, Kyoto 610-1101, Japan. Copyright © 2000 by National Stroke Association 1052-3057/00/0905-0007$3.00/0 doi:10.1053/jscd.2000.9886
250
Case Report A 34-year-old woman had experienced recurrent attacks of left motor hemiparesis for 2 years. The attacks were occasionally evoked by rotation of the patient’s neck to the right. None of her family members has suffered from cerebrovascular and/or coronary disease. This nonsmoking patient, who was not diabetic, hypertensive or hyperlipidemic, showed no neurologic deficit at the time of admission. Inspection of her head and neck uncovered no abnormality, and cervical bruit was not audible. Neither leukocytosis nor abnormally high C-reactive protein was seen in the laboratory data. Platelet aggregation had been controlled to between 33% and 48% for 18 months after administration of 200 mg/day of ticlopidine hydrochloride had been begun. The results of both electro- and echocardiogram were within normal limits. Chest radiographs showed no lesion or abnormal calcification. Magnetic resonance imaging (MRI) of the brain showed lacunar infarctions of the bilateral basal ganglia. Hypoperfusion of the frontotemporal region on the right side was demonstrated by cerebral blood flow (CBF) measurements by using technetium Tc99m hexyl-
Journal of Stroke and Cerebrovascular Diseases, Vol. 9, No. 5 (September-October), 2000: pp 250-253
ICA KINKING BY LYMPH NODE
methyl propylene amineoxine single photon emission computed tomography (99mTcHMPAO SPECT). No microemboli were detected by Doppler sonography. The right common carotid angiography disclosed a stenotic kinking of the ICA, which appeared redundant, about 15 mm distal to the carotid bifurcation (Fig 1). Cross circulation from the left carotid and vertebrobasilar systems through the anterior communicating artery and the right posterior communicating artery was seen. The patient had been asymptomatic for 20 minutes during balloon test occlusion of the right ICA. Because of these findings, a preoperative diagnosis of TIA due to stenotic kinking of the ICA caused by atherosclerosis was made, and the oral antiplatelet agent was continued.
251
The patient underwent exploration of the right ICA for a planned endarterectomy, when an enlarged firm lymph node (⬃15 mm in diameter) was found to have compressed and encroached the artery (Fig 2A). The vessel was tethered caudally and kinked by the lymph node; this was the finding that appeared on the angiogram as a redundancy. Dissection and removal of that lymph node, which adhered to the adventitia of the ICA and the surrounding tissue, was performed, resulting in only about a 10% increase of that carotid blood flow, as detected by intraoperative Doppler study. An arteriotomy showed that the lumen of that segment of the ICA, about 6 mm long, was grossly smooth and narrowed. Because atheromatous plaque was not found and the apparently indented ICA was already atrophic at the compressed part, an endarterectomy was not indicated. Instead, segmental resection (⬃10 mm) of the kinked, stenosed, and atrophic ICA followed by end-to-end reanastomosis was performed by microsurgery (Fig 2B). Pathological examination showed that the lymph node was inactive and calcified and was presumably the result of a previous inflammation. No neoplasm cells were found. The lumen of the resected segment of the ICA was narrowed, and atheromatous change was not evident. The atrophy of the vascular wall was localized around the compressed site. Vasculitis or fibromuscular dysplasia was not seen. The patient has continued to be asymptomatic for 3 years after the surgery. The oral antiplatelet agent had been stopped postoperatively. In the angiography performed 6 months after surgery, the anastomotic site of the ICA was confirmed to be widely patent and normally shaped (Fig 3). Postoperative CBF measurements showed that hypoperfusion of the right frontotemporal area disappeared.
Discussion
Figure 1. Preoperative angiogram of the right common carotid artery showing a stenotic kinking of the ICA, which appears redundant, about 15 mm distal to the carotid bifurcation.
The incidence of tortuousity, coiling, or kinking of the ICA has been estimated at 16% in a series of 1000 angiograms by Metz et al.4 It is reported that 4% to 16% of kinking of the ICA has stenosis.5 Cioffi et al6 found kinking of the ICA in 10.1% of 1010 unselected angiograms, whereas Najafi et al.7 reported a 5% incidence of this lesion in a series of 308 patients who underwent carotid surgery. There were 15 instances of kinking (4.8%) in the series of 312 carotid reconstructions performed by Vannix et al.3 A TIA caused by stenotic kinking of the ICA is not rare.3,8 According to Vannix et al.,3 kinking of the ICA is almost always accompanied by atherosclerosis, which may cause not only a hemodynamic ischemia, but also an embolic one. Although the stenosis of the ICA in this patient was less than 50% according to the North American Symptom-
252
K. NIIJIMA
Figure 2. Intraoperative microphotographs. (A) The kinking (arrow) and tethering of the ICA resulted from compression by the lymph node (LN), which has already been dissected. (B) Segmental resection and end-to-end reanastomosis of the ICA.
atic Carotid Endarterectomy Trial (NASCET) criteria,2 it was most probably responsible for the patient’s cerebrovascular events, based on the surgical outcome. A kinking of the ICA caused by compression by nonvascular masses, such as a parathyroid cyst, brachial cleft cyst, lipoma, cystic hygroma, neoplasm, substernal thyroid, thyroid adenoma, or an enlarged lymph node, was postulated,9 but has not been documented or reviewed in detail. Neurosurgeons and vascular surgeons may not infrequently encounter an enlarged lymph node during
dissection of the cervical ICA for carotid endarterectomy. To my knowledge, however, stenotic kinking of the ICA due to compression by a lymph node has never been reported. In the present case, both macro- and microscopic findings of the stenotic kinking in question suggest that long-standing extraluminal pressure by the calcified lymph node, rather than sclerotic redundancy, was the primary problem. It has been generally accepted that surgical interventions should be indicated in a stenotic kinking of
ICA KINKING BY LYMPH NODE
253
anastomosis of the ICA was considered to be the treatment of choice in this particular case.
References
Figure 3. Postoperative angiogram showing the patent ICA in normal shape.
the ICA, if the lesion is responsible for cerebrovascular insufficiency.7 It is important to presume an unusual cause of stenosis of the ICA when an atypical patient of TIA is encountered and a carotid surgery other than endarterectomy may possibly be worthwhile. Removal of the encroached calcified lymph node followed by resection of the atrophic segment and end-to-end re-
1. European Carotid Surgery Trialists’ Collaborative Group: MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet 1991;337:1235-1243. 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators: Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445-453. 3. Vannix RS, Joergenson EJ, Carter R: Kinking of the internal carotid artery: Clinical significance and surgical management. Am J Surg 1977;134:82-89. 4. Metz H, Murray-Leslie RM, Bannister RG, et al: Kinking of the internal carotid artery in relation to cerebrovascular disease. Lancet 1961;1:424. 5. Koskas F, Bahnini A, Walden R, et al: Stenotic coiling and kinking of the internal carotid artery. Ann Vasc Surg 1993;7:530-540. 6. Cioffi FA, Meduri M, Tomasello F, et al: Kinking and coiling of the internal carotid artery: Clinical statistical observations and surgical perspectives. J Neurosurg Sci 1975;19:15. 7. Najafi H, Javid H, Dye WS, et al: Kinked internal carotid artery. Arch Surg 1964;89:134. 8. Santon PE, McClusky DA Jr, Lamis PA: Hemodynamic assessment and surgical correction of kinking of the internal carotid artery. Surgery 1978;84:793-802. 9. Leipzig TJ, Dormann GJ: The tortuous or kinked carotid artery: Pathogenesis and clinical considerations: A historical review. Surg Neurol 1986;25:478-486.