Results of Carotid Re-Exploration for Post-Carotid Endarterectomy Thrombosis

Written By: Sam Savage

Published Date: December 7, 2007 Last Edited: December 7, 2007

By Hans, S S

Aim. Evaluate the results of carotid re-exploration for post- carotid endarterectomy (CEA) thrombosis associated with major neurological deficit. Methods. Data obtained from ongoing vascular registry. Retrospective analysis of 2216 consecutive CEAs performed in a single surgical practice.

Results. New neurological deficits developed in 53 patients (2.4%) following CEA. Fourteen patients sustained intraoperative stroke. Of 33 patients with postoperative stroke, nine patients had mild neurological deficit. Of the remaining 24 patients with postoperative stroke, five experienced intracerebral hemorrhage, three had strokes unrelated to operated artery, and one had stroke following control of bleeding from CEA patch disruption. The remaining 15 patients developed a significant neurological deficit following CEA and underwent re-exploration for postoperative carotid thrombosis. Five patients had minimal neurological improvement, five patients showed moderate recovery, and the remaining five patients had near complete recovery.

Conclusion. Prompt re-exploration for post CEA thrombosis associated with major stroke can result in satisfactory outcome in majority of patients.

KEY WORDS: Carotid stenosis – Endarterectomy, carotid – Stents.

Carotid artery thrombosis following carotid endarterectomy (CEA) often results in postoperative stroke after a lucid interval.113 Patients sustaining intraoperative stroke develop neurological deficit at the conclusion of operation without a lucid period. Intraoperative stroke is usually caused by artery-to-artery embolism or cerebral hypoperfusion during the period of carotid artery clamping.713 Patients experiencing intraoperative stroke should be evaluated by immediate carotid duplex scanning to ensure no technical problems at the endarterectomy site. In the absence of any duplex-defined abnormalities, such patients are generally best managed expectantly.6,8,12 Re-exploration is unlikely to yield any benefits and may be associated with increased morbidity in neurologically unstable patients. However, patients sustaining postoperative stroke (CEA thrombosis) with major neurological deficit should undergo immediate re-exploration to maximize salvage of neuronal function.6-13 The results of re-exploration of post-CEA thrombosis associated with significant neurological deficit were reviewed from an ongoing vascular registry in a single surgical practice.

Materials and methods

Retrospective analysis of 2216 consecutive carotid endarterectomies in a solo surgical practice from July 1980 to December 2004 was performed. Data were collected from an ongoing vascular registry. Indications for CEA included focal transient ischemic attacks/transient monocular blindness in 41% (902), asymptomatic high-grade stenosis in 24% (526), asymptomatic carotid stenosis with vertebrobasilar insufficiency in 21% (478), and prior stroke with good recovery in 14% (310). Endarterectomy was performed under general anesthesia in 90% of patients and under regional block in the remaining 10%. An intraluminal shunt was utilized in patients under general anesthesia if mean internal carotid artery (ICA) stump pressure was

Figure 1.- Causes of postoperative stroke.

Results

Fifty-three patients (2.4%) developed new neurological deficits following carotid endarterectomy: focal motor seizures (3), transient ischemic attack (3), intraoperative stroke (14), postoperative stroke (33). Modified Rankin scale to measure independence following stroke was used (Table I).14 Of 14 patients with intraoperative stroke, six had no or minimal improvement (Rankin Scale 4 or 5), three of these died, four had moderate recovery (Rankin Scale 3) and four had complete or near complete recovery (Rankin Scale 0, 1 or 2). Postoperative stroke (after a lucid interval) occurred in 33 patients. Nine of 33 patients with postoperative stroke had mild neurological deficit (slight hand weakness and/or dysphasia), thought to be associated with postoperative cerebral embolism. All nine patients had complete or near complete return of neurological function (Rankin Scale 0, 1 or 2). One patient had severe neurological deficit (Rankin Scale 5) following re-exploration for patch disruption associated with hemorrhage and died. Five patients developed intracerebral hemorrhage (two of these died), three patients had stroke unrelated to operated artery (contralateral hemisphere =2, brain stem infarct =1) – two died. Fifteen patients developed severe neurological deficit following a lucid interval of 30 minutes to 96 hours and underwent immediate re-exploration (within two hours of diagnosis). Indications for carotid endarterectomy in 15 patients were focal transient ischemic attack/transient monocular blindness =7, prior stroke with good recovery =1, asymptomatic with high-grade internal carotid stenosis (70%) =7 (of these, four had contralateral internal carotid artery occlusion). Nine were males and six were females with an age range of 47 to 82 years and mean age of 65 years. Thirteen patients had associated coronary artery disease, 11 had hypertension, one had diabetes mellitus, two had chronic obstructive pulmonary disease, and one had essential thrombocytosis. Fourteen patients had carotid endarterectomy under general anesthesia and one under cervical block. Distal intima was tacked down in two patients. Indwelling shunt was used in three, primary closure of endarterectomy was performed in 12, vein patch grafts in two and eversion endarterectomy in one patient. Completion arteriography was performed in 11 patients. Neurological deficit developed 30 minutes to 96 hours following CEA – within six hours in ten patients, six to 12 hours in two, 12-24 hours in two, and after four days (96 hours) in one. Nine patients had rather sudden onset of contralateral weakness of upper and lower extremity with involvement of speech and/ or visual field defect with rapid progression, stuttering neurological deficit (intermittent improvement) in four, and progressively worsening neurological deficit in two. All patients underwent immediate re-exploration without undergoing carotid/ cerebral arteriography.

TABLE I.-Modified rankin scale to measure disability following stroke.

TABLE II.-Causes of post-CEA thrombosis.

Re-operation

All re-operations were performed under general anesthesia with systemic heparinization. Distal internal carotid pulse was absent in 11 patients. Proximal clamp was applied about one inch proximal to the suture line. Upon opening the endarterectomy site, 11 patients were found to have complete occlusion with reddish-black thrombus and four patients had a small area of grayish-white platelet aggregates at the distal end. Removal of thrombus resulted in brisk retrograde bleeding in ten of 11 patients. Four patients with grayish-white thrombus (platelet aggregates) at CEA site had distal pulse. A #2 Fogarty catheter was passed very carefully into the distal internal carotid artery in one patient. Irrigation was performed with heparinized saline and indwelling shunt used in nine patients. In one patient, flow could not be re-established and the internal carotid artery was ligated. At re-operation, patch grafting was done in 14 patients (vein patch =11, Gore-Tex [Flagstaff, AZ USA] patch =2, Vascu-Guard [St. Paul, MN USA] patch =1). Interposition saphenous vein graft was performed in one patient. Resection of a short segment of common carotid artery was performed in one patient with kink of common carotid artery. Mean length of stay was 13-3 days (range 7-20 days). One patient developed syndrome of inappropriate ADH secretion. Postoperatively, all patients were placed on aspirin; two patients were placed on clopidogrel. There are varied causes of post-CEA thrombosis as depicted in Table II.

Functional assessment (modified rankin scale)

Patient functional status was independently assessed by a neurologist and a physiatrist at the time of discharge and was classified according to modified Rankin Scale.12 Five patients (33%) had minimal symptoms or residual weakness (Rankin Scale 0,1 or 2), five patients had moderate recovery with slight residual arm and leg weakness (Rankin Scale 3). All five patients received three to four weeks of physical/occupational and, if necessary, speech therapy in the rehabilitation unit of the hospital. Five patients had severe impairment (two died) (Rankin Scale 4 or 5). Two patients with Rankin Scale 5 were transferred to an extended care facility and one patient was discharged home with paramedical staff support. Recurrent stenosis developed in one patient five years following re- exploration and was treated with carotid stenting and aneurysmal change in the vein patch required open repair in the second patient six years after re-exploration. Discussion

A stroke following carotid endarterectomy may occur intraoperatively without lucid interval (intraoperative stroke) and is evident at the completion of the operation. Postoperative stroke occurs following a period of normal neurological function in awakening from CEA (lucid interval). Patients develop neurological deficit. An intraoperative stroke is usually caused by cerebral hypoperfusion or embolization to the brain, whereas a postoperative stroke is most often caused by a post-CEA thrombosis-embolism, and occasionally by intracerebral hemorrhage.713 Patients sustaining an intraoperative stroke should undergo an immediate carotid duplex scan. If the carotid duplex scan reveals technical problems at the endarterectomy site, the patient should undergo immediate re- exploration. Some authors recommend routine carotid re-exploration to rule out technical factors resulting in intraoperative stroke.10, 11 However, the results of re-exploration for an intraoperative stroke are worse than those for a postoperative stroke.10 Patients sustaining a mild postoperative stroke (slight extremity weakness and/or dysphasia) should be evaluated with a carotid duplex scan and a computed tomography (CT) scan of the head. These patients are generally treated non-operatively rather than by re-exploration as in a majority of patients, the cause of part of the neurological deficit is cerebra embolization and only occasionally carotid thrombosis.8 However, in patients with a postoperative stroke associated with a major neurologic deficit, immediate re- exploration should be performed. If the possibility of intracerebral hemorrhage (history of headache with or without seizures, sudden onset of severe motor deficit) exists in a patient with suspected post-CEA thrombosis, a non-contrast CT scan of the head should be performed. In the event the CT scan is negative for intracerebral hemorrhage, re-exploration of the endarterectomy should be immediately performed without resorting to carotid arteriography. Intraoperative assessment of the endarterectomy site following an endarterectomy closure should be performed prior to closure of the wound. A variety of techniques are available including continuous- wave Doppler wave insonation, duplex scanning and arteriography. In the event a technical defect (e.g. ICA stenosis, clamp defect or intimal flap) is detected, the artery can be reopened and the lesion corrected to prevent post-CEA, thrombosis and stroke.7-13 There were multiple causes of post CEA thrombosis in the present report. Completion carotid arteriogram detected a carotid artery spasm in one patient. In spite of the administration of papaverine, this patient developed a postCEA thrombosis with a stroke two hours following endarterectomy. Successful re-exploration with a thrombectomy of the endarterectomy site and PTFE patch grafting was performed. Completion arteriography revealed 20%-30% residual stenosis as a causative factor for post-CEA thrombosis in two patients. In retrospect, both patients should have had patch grafting at the initial endarterectomy. Operative findings, at the time of re-exploration, revealed an ICA/CCA kink in two patients and loose debris at the proximal endpoint in two other patients. In six instances, however, no obvious cause of post-CEA thrombosis could be determined. Perioperative stroke occurred in 51 (2.4%) patients in this series. Thirteen (25%) of these strokes occurred intraoperatively and the affected patients did not undergo re- exploration. Thirty-three patients had a postoperative stroke after an interval of normal neurologic function. Nine patients had a mild neurologic deficit and were not operated upon. Such a patient may be a challenge with regard to deciding whether to re-explore as what at first may appear to be a mild deficit may progress rapidly to a severe deficit which is indicative of an endarterectomy site thrombosis. The incidence of an endarterectomy site thrombosis resulting in a stroke, and results of re-exploration are similar to those reported by other investigators (Table III). A good neurological outcome can be expected in two-thirds of patients undergoing a re-exploration for post-CEA thrombosis.4,6,7,9-12 Previous reports and this study have emphasized technical causes resulting in a postcarotid endarterectomy thrombosis in the majority of instances.7-12 However, in some patients, the exact cause of post- CEA thrombosis could not be determined, in spite of liberal use of completion arteriography. Riles et al. have recommended that every effort should be made to prevent technical defects as the cause of a post-carotid endarterectomy.8 Correction of kink in the internal and common carotid artery and attention to the distal and proximal endpoints of the endarterectomy may help in the prevention of post- CEA thrombosis.8 In patients with a redundancy of the internal carotid artery following carotid endarterectomy, re-exploration with either plication of the internal carotid artery or resection of a short segment of the common carotid artery should be performed to prevent post-CEA thrombosis.8 If a small internal carotid artery or a high termination of plaque is encountered at the time of endarterectomy, patch closure should be performed to reduce the risk of immediate thrombosis. Patients with a mild neurological deficit following a CEA attributable to a postoperative embolism are treated non-operatively without re-exploration. However, in patients with a sudden onset of severe neurological deficit or with progressively worsening neurological deficit, immediate re-exploration for post- CEA thrombosis can result in a significant improvement in neurological function.

TABLE III.-Recent series investigating the incidence of endarterectomy site thrombosis.

Conclusions

Prompt re-exploration for post CEA thrombosis associated with major stroke can result in satisfactory outcome in majority of patients.

References

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2. Treiman RL, Cossman DV, Cohan JL, Foran RF, Levin PM. Management of post- operative stroke after carotid endarterectomy. Am J Surg 1981;142:236-8.

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4. Painter TA, Hertzer NR, O’Hara PJ, Krajewski LP, Beven EG. Symptomatic internal carotid thrombosis after carotid endarterectomy. J Vase Surg 1987;5:445-51.

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6. Koslow AR, Ricotta JJ, Ouriel K, O’Brien M, Green RM, Deweese JA. Re-exploration for thrombosis in carotid endarterectomy. Circulation 1989;80:73-8.

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9. Paty PS, Darling RC, Cordero JA, Shah BM, Chang BB, Leather RP. Carotid artery bypass in acute postendarterectomy thrombosis. Am J Surg 1996;172:181-3.

10. McKinsey JF, Desai TR, Bassiouny HS, Piano G, Spire, JP, Zarins CK et al. Mechanisms of neurologic deficits and mortality with carotid endarterectomy. Arch Surg 1996;131:526-32.

11. Radak J, Popovic AD, Radicevic S, Neskovic AN, Bojic M. Immediate re-operation for perioperative stroke after 2250 carotid endarterectomies: differences between intraoperative and early postoperative stroke. J Vase Surg 1999;30:245-51.

12. Rockman CB, Jacobowitz GR, Lamparello PJ, Adelman MA, Woo D, Schanzer A etal. Immediate reexploration for the perioperative neurologic event after carotid endarterectomy: is it worthwhile? J Vase Surg 2000;32:1062-70.

13. Sheehan MK, Greisler HP, Littooy FN, Baker WH. The effect of intraoperative duplex on the management of postoperative stroke. Surgery 2002;132:761-6.

14. Sulter G, Steen C. DeKeyserJ. Use of the Barthel Index and modified Rankin scale in acute stroke trials. Stroke 1999;30:1538- 41.

S. S. HANS

Department of Surgery

St. John Macomb Hospital

Warren, MI USA

Presented at the Western Surgical Association 2003 Annual Scientific Session. Loews Ventana Canyon Resort, Tucson, AZ USA, November 912, 2003.

Address reprint requests to: S. S. Hans, 28411 Hoover Road, 48093 Warren MI USA. E-mail [email protected]

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