Intracranial hemorrhage after carotid en

The only recognizable predisposing factor was relief of high-grade carotid stenosis greater than 90% whereas other factors such as age 58 to 81 years, preoperative hypertension systol

Intracranial hemorrhage

carotid endarterectomy

after

Frank B Pomposelli, M.D., Patrick J Lamparello, M.D., Thomas S Riles, M.D.,

Claude C Craighead, M.D., Gary Giangola, M.D., and A n t h o n y M Imparato, M.D.,

New York, N.Y

Among 1500 carotid endarterectomies performed between 1975 and 1984, 11 ipsilateral

intracranial hemorrhages (IH) occurred between the first and tenth postoperative days

for an incidence of 0.7% The mortality rate among these patients was 36% The only

recognizable predisposing factor was relief of high-grade carotid stenosis (greater than

90%) whereas other factors such as age (58 to 81 years), preoperative hypertension

(systolic blood pressure 120 to 160 nun Hg), preoperative head CT scans showing recent

infarction (only one in five positive), and preoperative cerebral infarction (only 1 of 11

patients) did not play a role All patients had normal coagulation studies No patient

required a shunt because all tolerated cross-damping o f the carotid artery Postoperative

systolic blood pressures were 200 to 240 mm Hg in 6 of 11 patients The time of

occurrence of IH extended from the immediate postoperative period to the tenth post-

operative day (mean interval 3.3 days) Treatment consisted ofcraniotomy in five patients;

four survived and one recovered completely Of the six patients treated nonoperatively,

three survived and two completely recovered IH shares equal incidence with recurrent

thrombosis, cross-clamping ischemia, and embolization as a cause ofperioperative stroke

Although all except IH can be prevented by current practice, the means of preventing IH

are not apparent; however, careful monitoring of blood pressure to prevent uncontrolled

hypertension deserves consideration (J VASe SuItG 1988;7:248-55.)

Reports from centers with large experiences in

carotid surgery have shown that carotid endarterec-

tomy can be performed with an overall stroke rate

of 2% to 3% At New York University, the post-

operative stroke incidence was 2.5% 1 The routine

use of local anesthesia with careful observation of the

awake patient together with an aggressive diagnostic

approach including angiography, CT scanning of the

brain, and ultimately exploration of the operative

sites has allowed us to identify the cause of the strokes

in 80% of patients Embolization, carotid throm-

bosis, hypotension, intracranial hemorrhage, and un-

certain causes each accounted for approximately

0.5% of perioperative stroke?

The early experience of Wylie et al.s and others ~-6

revealed the high likelihood of catastrophic intrace-

rebral hemorrhage in patients who had recently suf-

fered an acute stroke and underwent subsequent ca-

rotid endarterectomy to relieve total occlusion or

From the Division of Vascular Surgery, New York University

Medical Center

Presented at the Forty-first Annual Meeting of the Society for

Vascular Surgery, Toronto, Ontario, Canada, June 9d0, 1987

Reprint requests: Patrick ] Lamparello, M.D., New York Uni-

versity Medical Center, Division of Vascular Surgery, 550 First

Avenue, New York, NY 10016

248

high-grade stenotic lesions of the ipsilateral internal carotid artery Animal studies of Meyer 7 and Harvey and Rassmussen 8 supported the contention by Wylie

et al that endarterectomy in those circumstances con- verted an ischemic infarct into a hemorrhagic one, principally because of the damage to arterioles and capillaries by major cerebral arterial occlusions

On the basis of these observations, the attempts

to open totally occluded internal carotid arteries xi, the presence of recently completed stroke were largely abandoned Empirically, carotid surgery was delayed 4 to 6 weeks after completed stroke in pa- tients with stenotic lesions This proved to be successful in decreasing the incidence of cerebral hemorrhage after endarterectomy in these patients; however, occasional cases were still seen Patients with very stenotic carotid lesions, anticoagulation with heparin 9 or warfarin, 1° or uncontrolled hyper- tension 11 had risk factors previously discussed in the medical literature Recently there have been reports

of intracerebral hemorrhage in patients without ap- parent previous cerebral infarctions, who were not given anticoagulants and who were normotensive af- ter relief of high-grade stenosis of the ipsilateral in- ternal carotid artery.~2,1s This prompted review of our experience with intracranial hemorrhage after carotid endarterectomy in a series of 1500 procedures per,,"

Volume 7

Number 2

Table I Preoperative clinical data summary and procedure

Preoperative

50 (R)

60 (R)

80 (L)

40 (L)

70 (L)

60 (L)

90 (L)

60 (R) TIA = transient ischemic attack; AF = amaurosis fugax; CE = carotid endarterectomy; ND = no data

formed over a recent 10-year period (1975 to 1984)

at New York University Medical Center

The purpose of this article is to identify the factors

that place patients most at risk for intracranial hem-

orrhage after carotid endarterectomy, discuss possi-

ble pathophysiologic mechanisms, and describe our

principles for diagnosis and management of this dif-

ficult problem

M A T E R I A L A N D M E T H O D S

Among 1500 carotid endarterectomies consecu-

tively performed between 1975 and 1984 on the

vascular surgical service at New York University

Medical Center, 11 patients were identified who sus-

tained a perioperative stroke because of an ipsilateral

intracranial hemorrhage The hospital charts of these

patients were reviewed The age, sex, indication for

surgery, symptom-free interval before endarterec-

tomy, and preoperative CT scan findings were re-

corded

All patients underwent preoperative biplane ar-

terial angiography The degree of stenosis in the ca-

rotid arteries was determined by measurement of the

transverse luminal diameter of the involved vessels as

visualized on the arteriogram Ten operations were

done with cervical block anesthesia and one with

general endotracheal anesthesia No shunts were

used All patients remained neurologically intact dur-

ing carotid cross-clamping The one patient operated

on while under general anesthesia was initially given regional cervical block anesthetic This patient was neurologically intact with carotid cross-clamping and was placed under general anesthesia halfway through the carotid endarterectomy because of discomfort All patients received 3000 units of intravenous hep- arin before carotid cross-clamping; this was not re- versed All patients receive aspirin 325 mg/day and dipyridamole 75 mg/day preoperatively Five pa- tients received aspirin 325 mg/day and dipyridamole

75 rag/day postoperatively One patient was given heparin before surgery, but this was discontinued in the postoperative period

The blood pressure at admission, maximal intra- operative blood pressure, and maximal blood pres- sure before occurrence of cerebral hemorrhage were noted All patients had radial intra-arterial pressure monitoring performed in the operating room and recovery room

The time period between surgery and hemor- rhage influenced subsequent management Patients who had stroke in the recovery room were imme- diately operated on again If the carotid arteries ap- peared pulsatile, intraoperative carotid angiograms were obtained to rule out irregularities at operative sites that could have been the source of emboli Pa- tients whose deficits occurred later underwent non- invasive evaluation with ocular photoplethysmogra- phy and/or duplex scan, angiography, CT scan, or

250 Pomposelli et al

VASCULAR SURGERY

mm Hg

2 4 0 l

2 2 0 "

2 0 0 "

1 8 0 -

1 6 0 "

H O "

120 "

IO0 "

8 0 -

6 0 -

4 0

i , i , , , ,

2 3 4 5 6 7 8 I 0

PATIENT Fig 1 Preoperative blood pressure at admission

mmHg

2 4 0 -

2 2 0 "

1 8 0 -

1 6 0 -

1 4 0 ,

120 "

I 0 0 -

8 0 -

6 0 -

4 0 -

-1

, , , i , , , , , , ,

I 2 3 4 5 6 7 8 9 I 0 II

PATIENT Fig 2 Maximally reached intraoperative blood pressure

some combination o f these Some patients under-

went craniotomy Eventual outcomes in all cases were

determined

R E S U L T S

The patients ranged in age from 58 to 81 years

There were five men and six women The presenting

symptoms were transient ischemic attack in seven

patients, previous cerebral infarct in one, amaurosis

fugax in another, and nonfocal symptoms in two

Prothrombin time, partial thromboplastin time, and

platelet count were normal in each patient All had

90% or greater stenosis of the appropriate internal

carotid artery and six had 99% stenosis Several had

significant lesions in the contralateral internal carotid

artery Six patients had preoperative CT scans, four

of which were normal One scan was consistent with

mm Hg

2 4 0

2 2 0 - -

2O0

~80 1 -

160

~40

120 I00

8 0

6 0

4 0

I

2 3 4 5 6 7 8 9 I0 II

PATIENT Fig 3 Maximal blood pressure in postoperative period before intracerebral hemorrhage

recent infarction in the ipsilateral hemisphere and carotid endarterectomy was delayed 30 days One CT scan revealed an old ipsilateral infarct Five patients operated on early in the series had no CT scan pre- operatively, but all were neurologically intact at the time of operation The symptom-free interval before surgery ranged from 1 to 30 days but was at least

1 week in eight of nine patients with focal cerebral ischemia (Table I)

Three patients were taking antihypertensive med- ications preoperatively, but none had a preopera- tive blood pressure greater than 160/90 m m H g (Fig 1) Intraoperatively 9 of 11 patients became moderately to severely hypertensive (systolic 200 m m

Hg or greater) with carotid cross-clamping (Fig 2) Blood pressure was not artificially elevated with drugs No patient had a neurologic deficit intra- operatively During the postoperative period 5 o f !1 patients remained moderately or severely hyper- tensive before diagnosis of cerebral hemorrhage (Fig 3)

Hemorrhage occurred between 1 and 10 days postoperatively for a mean of 3.45 days One patient showed symptoms in the recovery r o o m and was immediately returned to the operating room An in- traoperative arteriogram was normal in this patient One other patient had repeat surgery after symptoms developed o n the third postoperative day and also had a normal intraoperative arteriogram Five other patients also underwent cerebral angiography and all had patent carotid arteries (Table II)

The presenting symptoms of cerebral hemorrhage are shown in Table II Hemiparesis was the most

Volume 7

Number 2

Table II Summary of course of patients after cerebral hemorrhage

Surv def

tion crani Surv def

Comp rec

Comp rec

(L) Hemi

Died

(R) Hemi

Sz Coma

Died

HA = headache; Hemi = hemiparesis; Sz = seizure; def = deficit; Comp rec = complete recovery; Crani = craniotomy; Hem = hematoma; Surv = survived

common Only five complained of headache Three

patients suffered seizures In two patients early in

this series the diagnosis was made by postmortem

examination in one patient and by a combination of

findings of hypertension, coma, dilated pupils, flaccid

exremities after a seizure, and bloody cerebral spinal

fluid on a lumbar puncture in the other Nine of the

11 patients had CT scans postoperatively Nine CT

scans demonstrated intracranial hematoma ipsilateral

t0 the side of surgery; eight showed intracerebral

hematoma and one scan demonstrated a subdural

hematoma (Table II)

Four patients died Five patients underwent cra-

niotomy and four survived, but only one completely

recovered The indications for craniotomy were

based on neurosurgical criteria These included a pro-

gressing neurologic deficit despite medical therapy

with mass effect on the CT scan from a surgically

accessible hematoma Only three of the seven sur-

vivors had minimal or no deficits (Table III) Overall

the survival rate of postoperative cerebral hemor-

rhage was 64% (seven patients)

Table III Eventual outcome of patients on the basis of type of therapy

No of patients Recovery Deficit Death

D I S C U S S I O N

Reports from centers with large experiences in carotid surgery have consistently demonstrated that carotid endarterectomy can be performed with a peri- operative stroke rate of 2% to 3%, but rarely is the mechanism of perioperative stroke described We have found that performing carotid endarterectomy

in the awake patient with continuous assessment of neurologic status and selective use of shunting on the basis of the patient's ability to tolerate carotid cross- clamping together with aggressive evaluation of postoperative deficits has identified embolization, thrombosis, hypotension, cerebral hemorrhage, and uncertain origin as equally occurring causes of peri-

252 Pomposelli et al

Journal of VASCULAR SURGERY

operative strokes 2 Although presently available tech-

niques can prevent strokes caused by most of these

mechanisms, the means of prevention of cerebral

hemorrhage afterendarterectomy remains unknown

Normal brain possesses the capability of resisting

changes in blood flow caused by variations in blood

pressure by the reflex contraction ofintracerebral ves-

sels as pressure increases and their relaxation as it

decreases? 4 In ischemic brain this autoregulatory

mechanism is lost and vessels tend to remain maxi-

mally dilated The use of positron emission tomog-

raphy in focal cerebral infarction has shown a zone

ofischemic, but viable brain surrounding the infarct,

which has been labeled the "ischemic penumbra "is

Vasodilation in this area leads to enhancement on

contrast CT scanning Lassen 16 dubbed this "luxury

perfusion" and suggested that it might be duc to local

metabolic alterations, that is, acidosis from anaerobic

metabolism Animal studies performed by Waltz ~7

suggest that in these areas of cerebral vasodilation

blood flow becomes passively dependent on blood

pressure Harvey and Rassmusscn s showed that

greatly fluctuating blood pressure in ischemic areas

of brain could lead to hemorrhage, suggesting that

the combination of autoregulatory paralysis and hy-

pertension can greatly increase perfusion and precip-

itate vascular disruption in these areas

Several authors have suggested that a similar

mechanism is responsible for paralysis of autoregu-

latory mechanisms in cerebral hemispheres of pa-

tients with near-occlusive carotid stenosis Cerebral

perfusion studies performed by Sundt et al.18 in pa-

tients with high-grade carotid stenosis revealed ab-

normally low blood flow to the ipsilateral cerebral

hemisphere Removal of the near-occlusive lesions

by endarterectomy resulted in increases in blood flow

of three to four times normal flow in some cases

This same category of patients occasionally manifests

postoperative neurologic dysfunction characterized

by severe temporal headache, nausea, vomiting, and

seizures Reigel et al?9 recently reported 10 patients

with this symptom complex after relief of high-grade

carotid stenosis These patients uniformly demon-

stratcd periodic lateral izing epileptiform discharges

on the ipsilateral side of the brain on electroenceph-

alograms obtained in the postoperative period and

suggested that these were a marker for its occurrence

Bernstein et al.~2 reported a case of a man who

died of a massive cerebral hemorrhage 6 days after

correction of an asymptomatic high-grade ipsilateral

carotid stenosis Preoperative neurologic examina-

tion and CT scan were normal In the postoperative

period he was normotensive and not taking heparin

or warfarin, but complained of severe headaches Postmortem examination of the brain revealed his- topathologic changes consistent with malignant hy- pertension in the hemisphere distal to the carotid endarterectomy whereas in the contralateral hemi- sphere pathologic findings were normal They sug- gested that cerebral hyperperfusion led to these his- tologic findings, although others 2° have disputed this

It has been our policy to delay carotid surgery for 1 month in patients with acute frank infarction and carotid stenosis Previously, patients with infre- quent transient ischemic attacks, amaurosis fugax, or who were asymptomatic did not necessarily have pre- operative CT scans if found to be clinically intact with a neurologic examination In recent years most

of our patients have had preoperative CT scans, al- though the discovery of an occult cerebral infarct ha~ not necessarily delayed surgery In five patients op- erated on during the earlier part of this study, no CT scan was obtained preoperatively, but all patients were neurologically intact with stable symptoms at the time of operation

All of our patients except those with specific con- traindications, receive 325 mg of aspirin and 75 nag

of dipyridamole daily postoperatively Heparin and warfarin are not used postoperatively except where specific strong indications exist (i.e., patients with prosthetic heart valves) No patient in this group was taking heparin or warfarin after operation

Hypertensive patients with blood pressure con- sistently greater than 160/90 m m H g on multiple determinations who require carotid endarterectomy have surgery delayed until blood pressure is con- trolled Diuretics, beta blockers, calcium channel blockers, and vasodilators are used to stabilize these~ patients preoperatively Despite this, we frequently see intraoperative hypertension with carotid cross- damping in the conscious patient (75% of patients) Postoperatively, hypertension has been uncommon (less than 5%) in our patients, although when it does occur, we attempt to keep the systolic blood pressure below 180 m m Hg From 1975'to 1983, intravenous hydralazine in doses of 5 mg was used for blood pressure control after carotid endarterectomy From

1984 until the present, intravenous metoprolol 10

to 15 nag every 12 hours is our drug regimen Five

of 11 patients (Fig 3) had postoperative blood pres- sures greater than 180 m m Hg despite use of this drug regimen We note that these patients were the exception to our usual experience

Four of the patients in this study were both neu- rologically intact and had normal preoperative CT

Volume 7

Number 2

February 1988 Intracranial hemorrhage after carotid endarterectomy 253

scans All tolerated surgery and initially did well Two

were never hypertensive postoperatively Two com-

plained of headache before showing signs of intra-

cranial bleeding It becomes apparent from these ob-

servations that normotensive, neurologically intact

patients without demonstrable cerebral infarction or

hypertension can also have cerebral hemorrhage after

endarterectomy The single factor that appears to link

all 11 patients was the relief of high-grade (90%) or

critical (99%) carotid stenosis

From these observations it would appear that the

blood brain barrier is overcome from rapid increases

in blood flow that occur after carotid endarterectomy

done for high-grade stenosis Moreover, severe hy-

pertension (Fig 3) may serve to increase the likeli-

hood of disruption of the blood-brain barrier with

resultant intracranial hemorrhage It remains un-

known why only a small fraction of patients with

high-grade carotid stenosis have cerebral hemorrhage

after endarterectomy, although the apparent fre-

quency of contrallateral high-grade lesions or total

occlusions that we and others ls'19 have observed sug-

gests that the status of the contralateral carotid artery

may bc a necessary factor

It is important to recognize that cerebral hem-

orrhage after endarterectomy, although rare, is an

important cause of postoperative neurologic deficit

that may occur in the absence of headache, nausea,

seizures, and other signs associated with intracranial

bleeding Since effective treatment is available, and

patients can recover without permanent disability, it

is important that all new postoperative neurologic

deficits, no matter how trivial, be expeditiously in-

vestigated Our present rationale for evaluation of

perioperative strokes has been described previously 2

Briefly, all major deficits occurring in the recovery

room mandate immediate reexploration A clinical

assessment is then made of arterial patency If the

artery appears patent, intraoperative angiography is

performed to look for correctable technical errors or

nonoccluding thrombus Major deficits occurring

later require emergency angiography or reexplora-

tion and intraoperative angiography if a significant

time delay (greater than 6 hours) is anticipated before

a routine angiogram can be performed Minor tran-

sient symptoms can be initially evaluated by nonin-

vasive studies if available, but angiography should

still be performed if they are not, and obviously in

all patients in whom they show abnormalities CT

scans are also obtained in these patients Patients with

surgically correctable technical defects or thrombosis

of their arteries are usually operated on unless CT

scan reveals a new infarct or hemorrhage Patients

with normal angiograms who have symptoms of stroke and hypertension should be suspected of hav- ing hemorrhage even in the absence of headache When an intracranial hemorrhage is discovered, neu- rosurgical consultation should be obtained Initially, patients are treated medically with blood pressure control Patients with a progressing deficit, with mass effect demonstrated on the CT scan, from a hema- toma in a surgically accessible location, are candidates for craniotomy and evacuation of the hematoma In our series this strategy resulted in a survival rate of 66% and complete recovery in 27% of patients

In summary, we have observed postoperative in- tracranial hemorrhage in 0.5% to 0.7% of patients undergoing carotid endarterectomy It accounts for approximately 20% of perioperative strokes The most prominent risk factor other than recent cerebral infarction is surgical relief of high-grade carotid ste- nosis Patients who are hypertensive, both intra- operatively and postoperatively, or where there is difficulty controlling postoperative hypertension are

at added risk Normotensive, neurologically intact patients without demonstrable cerebral infarction are also at risk with relief of high-grade carotid stenosis Postoperative intracranial hemorrhage mandates the same expeditious and aggressive evaluation as other causes of perioperative stroke Although mor- bidity and mortality rates remain high, careful med- ical management or neurosurgical intervention can save selected patients even in the face of severe neu- rologic deficits

R E F E R E N C E S

1 Imparato AM, Ramirez A, Riles TS, Mintger R Cerebral protection in carotid surgery Arch Surg 1982; 117:1073-8

2 Imparato AM, Riles TS, Lamparello PJ, Ramirez A The management of TIAs and acute strokes after carotid endar- terectomy In: Bernhard VM, Towne JF, eds Complications

in vascular surgery New York: Grune & Stratton, Inc, 1985:725-38

3 Wylie EJ, Hein MF, Adams JE Intracranial hemorrhage fol- lowing surgical revascularizatioan for treatment of acute strokes )" Neurosurg 1954;21:212-5

4 Breutman ME, Fields WS, Crawford ES, DeBakey ME Ce- rebral hemorrhage in carotid artery surgery Arch Neurol 1963;9:458-67

5 Gonzalez L, Carson ML Cerebral hemorrhage following suc- cessful endarterectomy of the internal carotid artery Surg Gynecol Obstet 1966;122:773-7

6 Hass WK, Claus RH, Goldberg AF, Johnson AL, Imparato

AM, Ransohoff J Special problems associated with surgical and thrombolytic treatment of strokes Arch Surg i966; 92:27-31

7 Meyer JS Importance ofischemic damage to small vessels in experimental cerebral infarction Neuropath Exp Neurol 1958;17:571-84

254 Pomposelli et al

Journal of VASCULAR SURGERY

8 Harvey J, Rassmussen T Occlusion of the middle cerebral

artery Arch Neurol Psychiatr 1951;66:20-9

9 Sundt TM The ischemic tolerance of neural tissue and the

need for monitoring and selective shunting during carotid

endarterectomy Stroke 1983;14:93-7

10 Takolander RJ, Bergqvist D Intracerebral hemorrhage after

internal carotid endarterectomy Acta Chir Scand 1983;

149:215-20

11 Caplan LR, Skillman I, Ojemann R, Fields WS Intracerebral

hemorrhage following carotid endarterectomy A hyperten-

sive complication? Stroke 1978;9:457-60

12 Bernstein M, Fleming JFR, Beck JHN Cerebral hyperper-

fusion after carotid endarterectomy A cause of cerebral hem-

orrhage Neurosurgery 1984;15:50-6

13 Solomon RA, Loftus CM, Quest DO, Lorrel JW Incidence

and etiology of intracerebral hemorrhage following carotid

endarterectomy J Neurosurg 1986;64:29-34

14 Hachinski V, Norris JW The vascular infrastructure In:

Hachinski V, Norris JW The acute stroke Philadelphia: FA

Davis Co, 1985:27-40

15 Hachinsld V, Norris JW The reversibility of cerebral isch- emia In: Hachinski V, Norris JW The acute stroke Phila- delphia: FA Davis Co, 1985:41-63

16 Lassen WA The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localized within the brain Lancet 1966;2:1113-5

17 Waltz AG Effect of blood pressure on blood flow in isch- emic and non-ischemic cerebral cortex Neurology 1968;18: 613-21

18 Sundt TF, Sharbrough FW, Piepgras DG, Kearns TP, Mes- sick IM, O'Fallon WM Correlation of cerebral blood flow and electroencephalographic changes during carotid endar- terectomy Mayo Clin Proc 1981;56:533-43

19 Reigel MM, Hollier LH, Sundt TF, Piepgras DG, Shar- brough FW, Cherry KJ Cerebral hyperperfusion syndrome:

a cause of neurologic dysfimction after carotid endarterec- tomy J VASe SURG 1987;5:628-34

20 Schroeder T, Sillesen H, Boesen J, Lanrsen H, Sorenson PS Intracerebral hemorrhage after carotid endarterectomy Eur

J Vasc Surg 1987;1:51-60

D I S C U S S I O N

Dr Jesse E T h o m p s o n (Dallas, Tex.) Cerebral hem-

orrhage now is a rare complication o f carotid endarterec-

tomy Dr Imparato's group has documented only 11 cases

in 10 years, an average o f one per year However, when it

occurs, it is a devastating event

About 25 years ago we all learned that patients with

acute profound strokes with totally occluded or tightly

stenotic carotid arteries operated on early suffered a high

rate of hemorrhagic infarction with a prohibitive mortality

rate These patients are no longer operated on and are not

the patients we are discussing here

Interestingly, o f the 11 patients, Dr Pomposelli has

analyzed only one who had a previous remote infarct,

whereas all the others had TIAs or nonlocalizing symp-

toms All had intraoperative hypertension, whereas 6 o f

the 11 patients had postoperative hypertension

I analyzed a recent 10-year experience o f our group of

918 endarterectomies and could identify with certainty

only four cases of cerebral hemorrhage, two in patients

with remote strokes and two with TIAs All had tight

stenoses, three had severe hypertension, and all four died

Our operative routine differs from the authors' in that

we use general anesthesia, employ a shunt routinely, and

inject dexamethasone (Decadron) intravenously immedi-

ately before carotid cross-clamping

In none of the 11 cases reported by Dr Pomposelli

was a shunt used Although no demonstrable neurologic

deficit was noted during carotid cross-clamping with the

patients awake, I wonder whether some ischemia may have

occurred

Prolonged ischemia followed by reperfusion results in

an increase in oxygen-dependent enzyme metabolites,

which may be detrimental to the blood-brain barrier

The most constant factor in these cases was relief o f high-grade stenosis 'Sundt at the Mayo Clinic has dem- onstrated hyperperfusion with cerebral blood flows in- creasing three or four times baseline levels after removal

of such stenoses

We have documented such hyperperfusion with arte- riography in a patient with TIAs and a tight stenosis who had severe headaches and seizures after operation His post- operative arteriogram showed marked increased vascularity and hyperperfusion

Another most important factor associated with cerebral hemorrhage is postoperative hypertension Thus in cases with possible ischemic vascular damage, loss o f autoreg- ulation, reactive hyperemia, and hyperperfusion, the su- perimposition o f severe hypertension may well result ir~ vascular rupture and cerebral hemorrhage

At present, with careful monitoring and vigorous ther- apy, we can control postoperative hypertension H o w to protect or enhance the integrity of the blood-brain barrier

is the problem

Dr Pomposelli, do you think the use of a shunt would have any value? Would use o f steroids during cross- damping add any protection? Should we avoid postop- erative aspirin therapy? Finally, is routine preoperative CT scanning in every case worthwhile or justifiable?

Dr Pomposelli I thank Dr Thompson for his re- marks This study was undertaken because of our impres- sion that most causes o f perioperative neurologic deficit after carotid endarterectomy are avoidable by present-

ly available techniques However, cerebral hemorrhage, which represents 20% o f perioperative neurologic deficits

in our patients, is not preventable at the present time Indeed, despite a substantial amount of experimental an- imal work and clinical observation by Dr Sundt and others,

Number 2

cerebral hemorrhage has an undetermined mechanism in

patients who have not had previous -strokes

Dr Thompson, we do not believe that the routine use

of shunts will prevent this complication Experiences re-

ported from other institutions that have used both selective

and routine shunting have shown results similar to ours

In addition, we have found the development o f cerebral

ischemia with carotid cross-damping is not a subtle find-

ing; patients usually manifest severe symptoms,, either los-

ing consciousness or having a profound neurologic deficit

within seconds o f being clamped Most of our patients

who have had surgery without a shunt and do not show

signs o f cerebral ischemia have ultimately done well even

with significant stenosis

We have, not routinely given our patients steroids I

am not aware o f any data to suggest that it will prevent

cerebral hemorrhage postoperatively

We routinely give our patients aspirin postoperatively

'Iowever, half of the patients in this series were not given

aspirin or dipyridamole postoperatively principally because

the hemorrhage occurred before the therapy would have

routinely been started In other studies that I am aware of, cerebral hemorrhage has occurred in patients who were and were not taking antiplatelet agents It is unclear whether or not aspirin usage should be continued routinely

in the postoperative period, although we have continued

to do so to avoid the possible deposition ofplatclet throm- bus on the endarterectomized area o f the carotid artery

We have not routinely obtained preoperative CT scans

on our patients because we believe that the neurologic status o f the patient and the clinical presentation are more important factors in determining risk and ultimate out- come In addition, we have not found that the discovery

o f an occult cerebral infarct in an otherwise asymptomatic

or stable patient has altered our treatment plan I am aware

of studies that have suggested that patients with asymp- tomatic stenosis or transient cerebral ischemia who have occult infarction shown on the preoperative CT scan are

• at an increased risk of stroke However, I do not know o f any studies that suggested there is an increased risk of cerebral hemorrhage in these circumstances