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Henry Ford Hospital Medical Journal

Volume 32 Number 3 Special Issue on Medical Computing Article 11

9-1984

Intracerebral Hemorrhage After Carotid Endarterectomy

José Biller

Andrew C. Hayes

Fred N. Littooy

William H. Baker

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Recommended Citation Biller, José; Hayes, Andrew C.; Littooy, Fred N.; and Baker, William H. (1984) " After Carotid Endarterectomy," Henry Ford Hospital Medical Journal : Vol. 32 : No. 3 , 197-203. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol32/iss3/11

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med j Vol 32, No 3, 1984 Case Reports

Intracerebral Hemorrhage After Carotid Endarterectomy

Jose Biller, MD,* Andrew C. Hayes, PA-C,** Fred N. Littooy, MD,** and William H. Baker, MD**

Intracerebral hemorrhage (ICH) is a rare complication operatively. The third patient, who was hypertensive, of carotid endarterectomy (CE). In our multicenter se­ had a nonfatal ipsilateral thalamic hemorrhage on the ries of 1,180 CE (Baker-Littooy), three ICH occurred, of third postoperative day. Though these three patients which two were fatal. One patient was receiving anti­ represent only 0.25% of our series, they constitute 12% coagulants because ofa prosthetic aortic valve; another of our total . ICH constitutes the largest per­ had rupture of a known ipsilateral intracranial an­ centage of nontechnically-related strokes and non- eurysm. Both occurred more than six weeks post­ cardiac deaths after CE.

after carotid endarterectomy is usually ascribed heparin, and a standard endarterectomy was performed to occlusion of the carotid artery, embolization, intimal through a lateral arteriotomy. Her immediate postoperative flap formation, or hemodynamic factors. Intracranial condition was satisfactory, and Doppler ultrasonic exam­ hemorrhagic complications after this procedure are ination was unremarkable. On the first postoperative day she considered rare. They embrace hemorrhagic , had a three-hour episode of and incurred a subendocardial anterolateral wall myocardial infarction. No intracerebral with or without ventricular or neurological abnormalities were noted then, but 36 hours subarachnoid penetration, and instances of hem­ later, when her was 190/80 mm/Hg, she de­ orrhagic cerebrospinal fluid associated with increased veloped left-sided weakness, left , left-sided as- . Bruetman and associates (1) re­ tereognosis, and a left homonymous visual field defect. CT ported six hemorrhagic complications among 900 showed a right thalamic hemorrhage with no interval change (0.66%) patients surgically treated for carotid stenosis or of the previously noted right parietal infarct (Fig. 3). occlusion. More recently Sundt, et al (2,3) noted five cases in a series of 1,145 (0.43%) carotid endarterec- Case 2 tomies. We noted three cases in our series of 1,180 A 70-year-old woman was admitted in October 1978 with a three-week history of ischemic rest pain in the left foot. Past (0.25%) carotid endarterectomies and report our expe­ medical history was remarkable for valvular heart disease, a rience in conjunction with a review of 36 previously thrombosed prosthetic aortic valve, previous left hemispheric published cases. transient ischemic attacks, arterial hypertension, and mellitus. Medications included NPH insulin, digoxin, Cou­ Case Reports madin, and dipyridamole. Ten days after a left femoropop­ liteal bypass, transient paralysis of the right upper and lower Case 1 extremities and confusion were noted. CT was obtained and A 63-year-oId woman was admitted in March 1983 for elective was normal. The next day she developed aphasia and right right carotid endarterectomy. Four weeks previously, she had hemiparesis. Repeat CT was unchanged. Partial recovery oc­ had an episode of and persistent left arm and leg curred over the next 24 hours. Cerebral arteriogram revealed numbness. Cranial computerized tomography (CT) at that 99% stenosis atthe origin ofthe left internal carotid artery with time revealed a right superior parietal infarction (Fig. 1). Cer­ an occluded middle cerebral artery stem (Fig. 4). Heparin was ebral arteriography demonstrated greater than 80% stenosis continued, and on November 7, 1978, a left carotid end­ of the origin of the right internal carotid artery (Fig. 2) and a arterectomy was performed under general anesthesia. small nonulcerated plaque at the origin of the left internal carotid artery. There was cross filling to the right side, and the Although the patient developed postoperative hypertension posterior cerebral arteries filled from the carotid injection. of 220 mm/Hg systolic (which required sodium nitroprusside The posterior circulation was unremarkable. The patient im­ for control), her neurological status improved. However, proved steadily. on the second day after endarterectomy, neurological dete­ rioration was evident, and CT showed a small infarction in the One month later, a right carotid endarterectomy was per­ formed under general anesthesia. At operation, inspection of the right carotid revealed an atheroma at its bifurcation. After Submitted for publication; june 4, 1984 it was opened, a stenotic was found with old and new Accepted for publication: july 19, 1984 clots situated on the intimal surface. Internal carotid artery Departments of Neurology^ and Surgery^^, Loyola University Medical Center back pressure was 86/60 mm/Hg with a mean of 70 mm/Hg; Address reprint requests to Dr, Biller, Division of , systemic pressure was 180/80 mm/Hg. The patient was given Department of Neurology, University of lowa, lowa City, lowa 52242,

197 Biller, Hayes, Littooy, and Baker

left (Fig. 5). She had significant recovery of neurological function and was discharged on the tenth postoperative day receiving Coumadin. Two months later she suffered sudden global aphasia, dense right hemiparesis, and lethargy. Prothrombin time was 19.8 seconds (N: 11.0-12.6 seconds), and CT revealed a large intracerebral located in the left temporal region extending into the external capsule (Fig. 6). She underwent successful removal of the hematoma and was discharged to a nursing home. Case 3 An 84-year-old woman experienced an episode of right mono­ cular blindness and transient left hemiparesis, but her neu­ rologic examination was normal. Blood pressure was 150/90 mm/Hg. Cerebral arteriography demonstrated severe stenosis of the internal carotid arteries bilaterally and an incidental 5 x 10 mm left internal carotid - posterior communicating junction . Aphasia developed after angiography when left carotid endarterectomy was performed. Back pressure was 32/29 mm/Hg with a systemic pressure of 198/76 mm/Hg. The aphasia gradually resolved, but seven months later she was found comatose and died the same day. Autopsy revealed that the previously noted aneurysm had ruptured. A previously unrecognized 2 mm aneurysm was found in the right middle cerebral artery, and a small cystic infarction had occurred in the left parieto-occipital junction (4). Fig. 1. Case 1. CT scan obtained at time of original symptoms demonstrates low density area in right superior parietal region consistent with an ischemic infarction.

Fig. 2. Case 1. Fig. 3. Case 1. Selective right carotid arteriogram demonstrates severe internal carotid CT scan obtained three days after right carotid endarterectomy, demon­ artery stenosis and ulceration. strates right thalamic hemorrhage. Area of prior infarction was un­ changed (not shown).

198 Intracerebral Hemorrhage After Carotid Endarterectomy

Fig. 6. Case 2. CT scan demonstrates large left lateral ganglionic hemorrhage with mass effect.

Fig. 4. Case 2. Selective left carotid arteriogram shows severe stenosis at origin of internal carotid and occlusion of middle cerebral artery system. Discussion Intracerebral hemorrhage following carotid end­ arterectomy is rare, and elevated blood pressure has usually been implicated as the primary risk factor. Hemorrhage most often occurs in the area of previous infarction, ipsilateral to the operation. In order to evaluate more completely the mechanism(s) of this complication, we have reviewed the reported cases of ICH after carotid endarterectomy. In addition to our three patients, we have reviewed 36 previously reported cases (1-3, 5-14), details of which are illustrated in the Table. During the past two dec­ ades, indications for carotid endarterectomy have changed, and some of these patients would not now be referred for surgery. Thirteen patients had operations to reopen occluded internal carotid arteries, most within days of a stroke. Three additional patients underwent surgery for severe internal within five days of a major stroke. For six patients, information about the severity of neurologic deficit and the timing of endarterectomy was incomplete.

Only 14 of these 36 patients had generally acceptable indications for operation. In three patients emergency Fig. 5. Case 2. surgery was undertaken for complications of an­ Immediate postoperative CT scan demonstrates small, enhancing infarct giography, and in one of these the carotid was found to in area of left basal ganglia. be occluded by a fresh . Among the remaining

199 Biller, Hayes, Littooy, and Baker

eleven cases, indications for operation were as follows: ninth postoperative month. In two patients the authors 1, nonfocal neurological symptoms; 7, hemispheric reported no discernible factor predisposing to hemor­ TIAs; 3, strokes (with surgery delayed 4-5 weeks). Ad­ rhage: one died at home, and the other underwent a mission blood pressure of ten patients was reported successful evacuation of the hemato ma. The time of and was greater than 170/95 mm/Hg in six subjects. At postoperative hemorrhage ranged from twelve hours to the time of the , hypertension seven months after endarterectomy. However, exclud­ was present in the four of whom it was reported. Ofthe ing two late hemorrhages, the average time to post­ five "normotensive" patients with hemorrhage, two operative was 3.4 days. Of the 36 cases, 34 were receiving , and one experienced (94.3%) died from the intracranial hemorrhage. rupture of a middle cerebral artery aneurysm in the

TABLE

Report of Cases of Intracerebral Hemorrhage After Carotid Endarterectomy

Blood Pressure Time Elapsed Reference CE Age/ at the time Between CE and Year Author Side Sex Indication of Admission Hemorrhage Course

1963 Bruetman, et al R 67 F TIAs/Left 158/90 mm/Hg 3 days died (1) hemiparesis after angiography

1963 Bruetman, et al R 52 M Completed 210/120 mm/Hg 4 days died (1) Stroke

1963 Bruetman, et al L 60 M Completed 160/100 mm/Hg 4 days died (1) Stroke

1963 Bruetman, et al R (,9 M TIAs 150/90 mm/Hg 6 days died (1)

Alive one month 1963 Bruetman, et al L 55 M TIAs 160/90 mm/Hg 6 days after evacua­ (1) tion of hematoma 1963 Bruetman, et al L 62 M TIAs 210/110 mm/Hg 5 days died (1)

1964 Wylie, et al R 50 M Stroke 138/92 mm/Hg 2 days died (12)

1964 Wylie, et al L ,->(> F Stroke 150/100 mm/Hg 2 days died (12)

1964 Wylie, et al E 49 F Stroke ? 12 hours died (12)

1964 Wylie, et al L 65 M Rind ? 3 days died (12)

1964 Wylie, et al R 63 F TIAs ? 36 hours died (12)

1965 Lyons R 67 M TIAs/Left 155/90 mm/Hg 3 days died (13) hemiparesis after angiography

1965 Lyons R .58 F TIAs 140/80 mm/Hg 36 Hours died (13) Obtundation

1965 Cole L 59 F Stroke 7 50 Hours died (14)

1965 Gurdjian, et al N/A N/A N/A N/A N/A died (15)*

1966 Gonzalez & L 70 M Stroke, obtunded 146/86 mm/Hg same day died Lewis (16) after

1966 Gonzalez & R 41 M Stroke 138/86 mm/Hg 24 hours died Lewis (16)

•Two patients sustained fatal hemorrhage into an area of infarction, one within 24 hours, the other within nine days.

Abbreviations: CE = carotid endarterectomy; TIA = transient ischemic attack; L = left; R = right; NA = not available; Ulc = ulcerated; Sten = stenosis; Occ = occlusion; RIND = reversible ischemic neurological deficit.

200 Intracerebral Hemorrhage After Carotid Endarterectomy

TABLE

Report of Cases of Intracerebral Hemorrhage After Carotid Endarterectomy (Continued)

Blood Pressure Time Elapsed Reference CE Age/ at the time Between CE and Year Author Side Sex Indication of Admission Hemorrhage Course

1966 Gonzalez & L 65 M Stroke 150/90 mm/Hg 24 hours died Lewis (16) 1966 Hass, et al R 68 M ? Stroke 3 days died (17) 1965 Rob** N/A N/A N/A N/A N/A died (18) R 1974 Ojemann, et al L 52 M TIAs 200/100 mm/Hg 4 days died (19) 180/100 mm/Hg L 1978 Caplan, et al R 57 F Stroke 180/100 mm/Hg 18 hours died (11) 1978 Caplan, et al L 45 F Stroke 165/95— 4 days died (11) 170/100 mm/Hg 1981 Sundt, et al L 74 M Near syncope, 160/90 mm/Hg 5 days died 1983 (2,3)*** blurred vision 1983 Takolander and L 68 F Stroke 200/110 mm/Hg 1 day died Bergqvist (20) 1983 Takolander and R 60 F TIAs 150/70 mm/Hg 6 days died Bergqvist (20) 1983 Takolander and R 69 M TIAs 170/85 mm/Hg 4.5 months died Bergqvist (20) 1983 Takolander and R-L 67 F TIAs > R CE; 6 wks died Bergqvist (20) Second Opera­ later L CE tion asymptomatic 1983 Takolander and R-L 73 F TIAs 200/100 mm/Hg 5 days after died Bergqvist (20) Second Opera­ second tion asymptomatic operation 1984 Present cases R 63 F Infarct 160/80 mm/Hg 3 days after alive 180/90 mm/Hg operation 1984 Present cases L 70 F Infarct 170/90 mm/Hg 2 months died six Incomplete months later resolution 1984 Present cases L 84 F TIAs 150/90 mm/Hg 7 months died

**Three patients with successful results from arterial reconstruction died of intracranial hemorrhage. ***This reference reports five cases, but only in one are clinical data available. Intracerebral hemorrhage occurred in five patients, and was fatal in four. Two were on heparin; two were receiving .

Abbreviations: CE = carotid endarterectomy; TIA = transient ischemic attack; L = left; R = right; NA = not available; Ulc = ulcerated; Sten = stenosis; Occ = occlusion; RIND = reversible ischemic neurological deficit.

Although its incidence is less than 1%, hemorrhage after Patient selection endarterectomy represents the largest cause of Three aspects of improper patient selection are clear: 1) nontechnically-related neurologic morbidity and non- operating soon after completed severe stroke, 2) re- cardiac mortality (1-3). Our experience and this review vascularizing a long-standing totally occluded internal of the literature indicate four major causative factors of carotid artery, 3) operating in the face of coincidental ICH after CE: improper patient selection, arterial hyper­ intracranial pathology. The first two aspects were fre­ tension, postoperative use of anticoagulants, and post­ quent causes of intracranial hemorrhage in the early operative hyperperfusion. carotid endarterectomy experiences. Today, reopening

201 Biller, Hayes, Littooy, and Baker

a chronically occluded artery is infrequently performed, hemorrhage, but noted that an increased cerebral and carotid endarterectomy after infarction with good blood flow (measured by xenon techniques) was a risk neurologic recovery is now usually deferred a minimum factor. They have labeled this postoperative increase in of 4-6 weeks. These changes reflect awareness of the cerebral blood flow the "hyperperfusion syndrome." risk factors involved. Concomitant intracranial pathol­ We did not measure the regional cerebral blood flow in ogy includes or mass . Even in the our patients, but none developed other clinical mani­ presence of these lesions, some patients may never­ festations common to this syndrome, or theless require endarterectomy. Cases 2 and 3 in this . Hypercarbic general anesthesia, report are examples of these risk factors. included as a possible cause of postoperative hyper­ tension, is of historical interest only. Hypertension and hyperperfusion Arterial hypertension following carotid endarterectomy Postoperative anticoagulation is a serious clinical problem with observed incidence Among the patients with ICH after CE reported by between 20% and 56% (15-17). These differences in part Sundt, et al (2,3), two were receiving anticoagulants, reflect the variable definition of hypertension. Caf- and two were receiving antiplatelet medications at the ferata, etal (18) consider hypertension asan elevation in time of hemorrhage. One of our patients with delayed systolic blood pressure greater than 40 mm/Hg above postoperative intracranial hemorrhage and one other baseline, while Towne and Bernhard (17) regard the reported patient were receiving anticoagulants when condition as a persistent rise in systolic blood pressure they experienced intracerebral bleeding after carotid to greater than 200 mm/Hg. We define hypertension as endarterectomy. In our patient, previous thrombus an elevation of blood pressure greater than 10% above formation by an aortic valve prosthesis had mandated the highest preoperative pressure. Assidao and associ­ this therapy. ates (19) noted that hypertension after carotid end­ arterectomy occurred more frequently among patients In summary, postendarterectomy hemorrhagic com­ with preoperative blood pressures greater than 170/95 plications have multiple causes. Hyperperfusion sec­ mm/Hg. Hypertension may result from carotid sinus ondary to revascularization of a severely stenotic artery baroreceptor dysfunction, neurogenic factors, or hy- and systemic hypertension play a predominant role. percarbic anesthesia (20). Bove, et al (15) observed that The use of anticoagulants or antiplatelet medications hypertension resultingfrom carotid sinus baroreceptor can be implicated in some cases. Inappropriate timing dysfunction peaked 2.3 hours after endarterectomy. of operation was a major cause of complicating intra­ This occurrence three days earlier than the average cranial hemorrhage early in the experience with carotid onset of hemorrhage (3.4 days in our review) suggests endarterectomy. Recognizing this led to changes in the that this cause of hypertension may not play an impor­ timing of and indications for the operation. After cer­ tant role in the hemorrhage. ebral infarction, regional changes may include hyper­ emia, venous congestion, diapedesis, vascular fragility, Neurogenic hypertension is believed to be a secondary and consequently intracerebral hemorrhage. These reflex rise in blood pressure, responding to an increase events may explain the time delay of hemorrhage after in intracranial pressure. It has been theorized that dur­ carotid endarterectomy. ing a previous , neurons and blood Although the major emphasis for safe carotid end­ vessels were hypoxic and hypoperfused and that restor­ arterectomy has been technical excellence and intra­ ation of full vascular pressure within the area leads to operative protection, postoperative intracerebral hemorrhage. Caplan and associates (5) advanced the hemorrhage constituted 12% of the strokes in our se­ theory that the vascular bed distal to severe arterial ries. Recognition of this problem and its causes may stenosis is protected from the effects of hypertension lead to safer operations. and that the reestablishment of higher perfusion pres­ sure leads to vascular rupture and hemorrhage. In our cases 1 and 2, there was evidence of hypertension in the Acknowledgments postoperative period. However, in case 1, the high The authors thank Bernadette Spurgeon and Joyce Will- carotid artery back pressure suggests that eliminating neff for manuscript preparation. the offending carotid lesion did not alter the regional pressure. Sundt, et al (2,3) found no association be­ tween changes in blood pressure and postoperative

202 Intracerebral Hemorrhage After Carotid Endarterectomy

References

1, Bruetman ME, Fields WS, Crawford ES, De Bakey ME, Cerebral 11 Hass WK, Clauss RH, Goldberg AF, Johnson AL, Imparato AM, hemorrhage in carotid artery surgery. Arch Neurol 1963;9:458-67, Ransohoff J, Special problems associated with surgical and thrombolytic treatment of strokes. Arch Surg 1966;92:27-31, 2, Sundt TM )r, Sharbrough FW, Piepgras DG, Kearns TP, Messick JM jr, O'Gallon WM, Correlation of cerebral blood flow and li. Rob CC, Operation of acute completed stroke due to electroencephalographic changes during carotid end­ of the internal carotid artery. Surgery 1969;65:862-5, arterectomy. With results of surgery and hemodynamics of cer­ ebral ischemia. Mayo Clin Proc 1981;56:533-43, 13. Ojemann R, Crowell R, Roberson G, Fisher CM, Surgical treat­ ment of extracranial carotid occlusive disease, Clin Neurosurg 3, Sundt TM Jr, Sharbrough FW, Peipgras DG, The significance of 1974;22:214-63, cerebral blood flow measurements during carotid end­ arterectomy. In: Bergan Jj, Yao JST, eds. Cerebrovascular in­ 14, Takolander RJ, Bergquist D, Intracerebral hemorrhage after in­ sufficiency. New York: Crune & Stratton, Inc, 1983:287-307, ternal carotid endarterectomy. Acta Chir Scand 1983;149:215-20,

4, Adams HP Jr, Carotid stenosis and coexisting ipsilateral intra­ 15. Bove EL, Fry WJ, Gross WS, Stanley JC, Hypotension and hyper­ cranial aneurysm, A problem in management. Arch Neurol tension as consequences of baroreceptor dysfunction following 1977;34:515-6, carotid endarterectomy. Surgery 1979;85:633,

5, Caplan LR, Skillman J, Ojemann R, Fields WS, Intracerebral hem­ 16, Lehv MS, Salzman EW, Silen W, Hypertension complicating car­ orrhage following carotid endarterectomy: A hypertensive com­ otid endarterectomy. Stroke 1970;1:307, plication? stroke 1978;9:457-60, 17. Towne JB, Bernhard VM, The relationship of post-operative hy­ 6, Wylie E|, Hein MF, Adams JE, Intracranial hemorrhage following pertension to complications following carotid endarterectomy. surgical revascularization for treatment of acute strokes, J Neuro­ Surgery 1980;88:575, surg 1964;21:212-5, 18, Cafferata HT, Merchant RF Jr, De Palma RG, Avoidance of post- 7, Lyons C, Progress report of the joint study of extracranial arterial carotid endarterectomy hypertension, Ann Surg 1982;196:465-72, occlusion. In: Sieckert RC, Whisnant JP, eds. Cerebral vascular 19, Asiddao CB, Donegan JH, Whitesell RC, Kalbfleisch JH, Factors disease: Transactions of the fourth conference, Princeton, NJ, associated with perioperative complications during carotid end­ New York: Grune & Stratton, Inc, 1965:221-39, arterectomy, Anesth Analg 1982;61:631-7,

8, Cole DS, Surgery in extracranial cerebrovascular disease, Br J 20, Eskind SJ, Dean RH, Blood pressure aberrations in carotid artery Surg 1965;52;892-901, surgery. In: Bergan JJ, Yao JST, eds. Cerebrovascular in­ 9, Gurdjian ES, Darmody WR, Lindner DW, Thomas LM, The fate of sufficiency. New York: Grune & Stratton, 1983:469-79, patients with carotid and vertebral artery surgery for stenosis or occlusion, Surg Gynecol Obstet 1965;121:326-30,

10. Gonzalez L, Lewis CM. Cerebral hemorrhage following suc­ cessful endarterectomy of the internal carotid artery. Surg Gyn­ ecol Obstet 1966:773-7,

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