Annals of Vascular Surgery
Volume 21, Issue 2 , Pages 172-177, March 2007

Recanalization of a Thrombosed Carotid Artery Following Endarterectomy

Department of Surgery, Division of Vascular Surgery, University of Southern California, Keck School of Medicine

Los Angeles, CA

Article Outline

 

Recanalization of perioperative carotid artery thrombosis following carotid endarterectomy, managed with anticoagulation therapy alone, has not been reported. We describe a case of a patient with symptomatic carotid artery stenosis who underwent endarterectomy. During the perioperative period, carotid artery thrombosis was discovered after an episode of amarousis fugax. Anticoagulation therapy was instituted, and during follow-up, the carotid artery recanalized.

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Introduction 

Perioperative thrombosis of the carotid artery following carotid endarterectomy (CEA) is an uncommon event. Reported perioperative neurologic event rates following CEA vary; however, those patients who do have an ipsilateral, perioperative neurologic event, thrombosis of the carotid artery is a common finding1 and is often felt to be the cause of the event.2, 3 The optimal management strategy for patients with perioperative carotid artery thrombosis is not well defined. This case supports the utility of anticoagulation therapy alone for the treatment of perioperative carotid artery thrombosis following CEA in select cases.

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Case 

A 56-year-old male was transported to an outside hospital after found unresponsive at his residence. At the outside hospital, the patient regained consciousness and was found to have bilateral high-grade internal carotid artery (ICA) stenoses by magnetic resonance angiography (MRA) and duplex scanning. On hospital day 3, he was transferred to the University of Southern California University Hospital (USC-UH) for further management.

On arrival to USC-UH, the patient was awake and conversant with mild left upper extremity and facial weakness. His past medical history was significant for poorly controlled hypertension. He was a nonsmoker, nondiabetic, and had normal total cholesterol. Bilateral carotid pulses were present with bruits. Carotid duplex scanning at USC-UH performed by a registered vascular technologist and reviewed by a board certified vascular surgeon indicated bilateral high-grade (>80%) stenosis of the ICA (Figs. 1A and B). A computerized tomography (CT) scan of the head showed evidence of an acute ischemic infarct in the right frontal lobe in the area of old infarct. There was no evidence of mass effect, midline shift, or hemorrhage. A CT angiogram of the extracranial arterial tree confirmed the findings from the outside hospital and documented normal intracranial arterial anatomy (Fig. 2, Fig. 3). Heparin and antiplatelet therapy (Aggrenox) were started.

Over a 2-week period the patient's neurologic deficits improved, and he was taken to the operating room for an uneventful right CEA using a shunt and Dacron patch. Intraoperative, completion duplex scanning showed normal flow dynamics in the distal common proximal external and proximal internal carotid arteries (Fig. 4). The patient was awakened from general anesthesia, extubated in the operating room, noted to be neurologically intact from baseline, and returned to the ward. Heparin was discontinued; Aggrenox was continued.

On postoperative day 4, the patient complained of a single transient episode of right-sided mono-ocular blindness. An immediate carotid duplex scan was performed that showed acute thrombosis of the right common external and internal carotid arteries (Figs. 5A, B and C). As the neurologic event was mild and transient, it was elected to treat the patient with anticoagulation therapy; systemic heparin therapy was initiated. Aortic arch angiography was performed 6 days after the event to assess the contralateral ICA and to confirm the duplex findings of the right carotid artery thrombosis. The left carotid system had greater than 90% stenosis of the ICA, and the entire right carotid system was thrombosed (Fig. 6).

There were no further neurologic events and 2 weeks after the right CEA, an uneventful left CEA with shunt, Dacron patch, and completion duplex scanning was performed. The patient had an uneventful recovery and was subsequently transferred to a rehabilitation facility on warfarin with the aim of maintaining an international normalized ratio between 2 and 3.

At 2 months postoperatively, the patient reported feeling a bounding pulsation in his right neck. On examination, the patient did indeed have a pulse over his carotid artery. Carotid duplex scanning demonstrated the previously thrombosed right carotid arteries to be patent without filling defects or stenosis (Figs. 7A-C). MRA of the carotid arteries confirmed these findings (Fig. 8). The patient was last seen at 16 months from his initial neurologic event. He is neurologically intact with bilateral patent carotid arteries without evidence of stenosis or defect.

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Discussion 

Acute ICA occlusion following endarterectomy is not known to be a common event. However, in those patients who do suffer a perioperative neurologic event following CEA, carotid artery thrombosis has been shown to be a common etiology. Edwards et al.1 reported on 27 patients with postoperative hemiparesis following CEA; 12 (44%) of these patients were found to have thrombosis at re-exploration. Rosenthal et al.2 reported on 12 patients with “immediate profound postoperative deficits” who underwent re-exploration and found seven (58%) to have a thrombosed carotid artery; Aburahma et al3 reported on 32 patients with perioperative neurologic events and found 19 (59%) patients to have carotid artery thrombosis.

Perioperative carotid artery thrombosis following CEA is generally felt to be due to technical error or platelet deposition3 in the absence of technical error. In Rosenthal's2 report, technical error was determined to be the cause of perioperative carotid artery thrombosis in three of the seven patients returned to the operating room, and platelet-fibrin aggregates was the only finding in the other four patients. The exact cause and timing of thrombosis in the case presented here is uncertain. Despite the patient's symptoms presenting on postoperative day 4, it is certainly possible that the thrombosis occurred earlier. With that said, technical error such as an intimal flap or ICA dissection must be considered as an etiology. However, on the completion duplex scan (see Fig. 4), no abnormality was noted. A dissection caused by the shunt in the more distal ICA is possible and would not necessarily have been appreciated on the completion duplex scan, but the follow-up MRA after spontaneous recanalization showed no evidence of distal dissection, and the duplex scan at that time was as well without abnormality. Therefore, spontaneous thrombosis due to platelet deposition is the likely etiology of perioperative carotid artery thrombosis following CEA in this case.

The optimal management strategy for perioperative carotid artery thrombosis following CEA is not well defined. Immediate re-exploration is recommended by many authors,2, 4, 5, 6 resulting in variable resolution of the neurologic deficit. In Rosenthal's2 report, after re-establishment of flow, two patients had immediate return of function, two had some slow improvement, one had no improvement, and two patients died of stroke-related causes. Other authors report similar variable recovery of neurologic function and mortality following re-exploration for perioperative carotid artery thrombosis following CEA (Table I). For patients with minor transient deficits following CEA, even in the setting of carotid artery thrombosis, nonoperative management is a reasonable and recommended management strategy.2, 7 The rationale behind this line of reasoning that influenced our decision to forgo re-exploration is that a minor neurologic event could be transformed into a major event with re-exploration due to the possibility of converting an ischemic infarct into a hemorrhagic infarct, or due to altering cerebral perfusion during re-exploration.5

Table I. Review of outcome of patients with neurologic deficit and re-exploration
AuthorNNo recoverySome recoveryFull recovery
Towne5050
Aburahma1257∗nr
Simma4103
Treiman85∗∗12

nr, not reported.

∗This includes patients with “complete and satisfactory resolution.”

∗∗2 of these patients died.

It goes without saying that thrombolytic therapy (systemic or catheter directed) for perioperative carotid artery thrombosis following CEA is contraindicated. However, one must not forget that thrombus itself is a potent activator of the body's natural fibrinolytic system. The efficacy of this system (without pharmacologic fibrinolytic therapy) is well documented. Archie8 reported a case of primary ICA thrombosis, diagnosed by angiography, which during follow-up recanalized itself via flow through the superior thyroid. In venous thrombotic events of the lower extremity, greater than 65% of thrombosed vein segments recanalize with anticoagulation only,9 and we have documented resolution of aortic mural thrombi with anticoagulation alone.10

This case documents the efficacy of the human body's in situ fibrinolytic system and supports nonoperative management of patients with perioperative, minor, transient neurologic deficits and carotid artery thrombosis following CEA. Anticoagulation therapy, which inhibits clot propagation, essentially empowers the fibrinolytic system to lyse clot and potentially restore flow. As illustrated in this case and also in aortic mural thrombi, the resolution of thrombus occurred in the setting of minimal arterial disease or stenosis. This suggests that in the patient with an acute thrombosis of a normal arterial segment that is accompanied by minimal to no symptoms of end organ ischemia, an alternative to surgical or thrombolytic intervention is anticoagulation alone. This could be particularly helpful in the clinical setting of a patient who has significant risk factors or contraindications to surgical or thrombolytic therapy.

In conclusion, this case demonstrates the remarkable ability of the body's fibrinolytic system, and supports nonoperative management of perioperative carotid artery thrombosis following CEA in select patients. Furthermore, the well-documented finding here of restoration of flow in the thrombosed carotid artery should serve as a reminder that during duplex scanning of the contralateral carotid artery, the thrombosed ICA should be interrogated and reconfirmed during follow-up.

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References 

  1. Edwards WH, Edwards WH, Mulherin JL, et al. The role of antiplatelet drugs in carotid reconstructive surgery. Ann Surg. 1985;201:765–770
  2. Rosenthal D, Zeichner WD, Lamis PA, Stanton PE. Neurologic deficit after carotid endarterectomy: pathogenesis and management. Surgery. 1983;94:776–779
  3. Aburahma AF, Robinson PA, Short YS. Management options for post carotid endarterectomy stroke. J Cardiovas Surg. 1996;37:331–336
  4. DeWeese JA. Management of acute strokes. Surgical Clinics of North America. 1982;62:467–472
  5. Towne JB, Bernhard VM. Neruologic deficit follwoing carotid endarterectomy. Surgery Gynecology & Obstetrics. 1982;154:849–852
  6. Simma W, Hesse H, Gilhofer G, Menner C, Muck G. Management of immediate occlusion after carotid reconstruction. J Cardiovas Surg. 1987;28:176–179
  7. Treiman RL, Cossman DV, Cohen JL, Foran RF, Levin PM. Management of postoperative stroke after carotid endarterectomy. Am J Surg. 1981;142:236–238
  8. Archie J. Internal carotid artery recannulation after thrombosis caused by atherosclerotic occlusion of the common carotid artery. Cardiovascular Medicine and Surgery. 1986;13:153–154
  9. Green D, Hirsh J, Heit J, et al. Low molecular weight heparin: a critical analysis of clinical trials. Pharmacological review. 1995;46:89–109
  10. Bowdish ME, Weaver FA, Liebman HA, et al. Anticoagulation is an effective treatment for arotic mural thrombi. J Vasc Surg. 2002;36:713–719

 Presented at the 23rd Annual Meeting, Southern California Vascular Surgical Society, La Quinta, California, May 13-15, 2005.

PII: S0890-5096(07)00065-9

doi:10.1016/j.avsg.2007.01.006

Annals of Vascular Surgery
Volume 21, Issue 2 , Pages 172-177, March 2007

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