1168

Atheromatous Pseudo-occlusion of theInternal Carotid Artery

Daniel H. O'Leary, MD, Heinrich Mattle, MD, and Jeffrey E. Potter, BS

Between 1978 and 1988, the diagnosis of atheromatous pseudo-occlusion of the internal carotidartery was made in 34 patients by angiography. Results of noninvasive tests were abnormal in33 of the 34 patients examined. Twenty-five patients had carotid endarterectomy, and the othernine were treated medically. Four of the 34 patients (12%) had significant complications, tworelated to angiography and two to surgery. Twenty-three of the 25 operated patients were seenin long-term follow-up; 19 (83%) were found to have a patent operated vessel by noninvasivetesting. None of the 23 operated patients followed up suffered recurrent neurologic deficitsfollowing surgery; two had distant contralateral strokes. Three of the nine patients treatedmedically (33%) experienced delayed ipsilateral stroke. This study shows that the risksassociated with angiography and surgery for atheromatous pseudo-occlusion are significant andare higher than previously reported. (Stroke 1989;20:1168-1173)

Highly stenotic but patent internal carotidarteries (ICAs) can easily be misdiag-nosed as occluded by both noninvasive

testing and by angiography. Blood flow distal to asite of extreme stenosis may be so minimal that itremains undetected. The term "atheromatouspseudo-occlusion" was first used by Lippman et alin 1970.] They described layering of contrast mate-rial along the dependent posterior wall of the ICAdistal to a site of high-grade stenosis at the time ofangiography. Other descriptive terms used to cate-gorize the angiographic appearance of suchextremely stenotic lesions are the poststenotic slimsign, the string sign, and the nearly occluded carotidartery.2-8 Once identified, urgent carotid endarter-ectomy seems to be automatically accepted as appro-priate for pseudo-occlusion. However, surgery forpseudo-occlusion should be attempted only if sur-gically treated patients are shown to have betterprognoses than those treated medically and if long-term patency of the operated vessel is high. Theseissues have not been previously addressed.

This report describes our experience with 34patients with atheromatous pseudo-occlusion. All34 underwent selective carotid angiography, and 25subsequently had carotid endarterectomy. We reporton the complications associated with both proce-dures. We also report the long-term clinical out-

From the Department of Radiology, New England DeaconessHospital and Harvard Medical School, Boston, Massachusetts.

Address for correspondence: Daniel H. O'Leary, Departmentof Radiology, Brigham and Women's Hospital, 75 Francis Street,Boston, MA 02215.

Received October 3, 1988; accepted lanuary 26, 1989.

come and long-term vessel patency of the operatedvessel in an attempt to address the issue of appro-priate management of patients with nearly occludedcarotid arteries.

Subjects and MethodsFrom July 1978 until July 1988, 1,092 successive

patients underwent angiography for suspected ex-tracranial cerebral vascular disease. The diagnosisof pseudo-occlusion was made in 34 patients (3%),16 men and 18 women, average age 66 (range47-78) years. Presenting symptoms were transientischemic attacks (TIAs) in 17, stroke in 14, andnonlocalizing symptoms in one; two patients wereasymptomatic. Risk factors included coronaryartery disease in 19, diabetes in 16, hypertensionin 22, peripheral vascular disease in 12, and hyperlip-idemia in three. Three patients had undergoneprevious endarterectomy of the pseudo-occludedvessel.

All 34 patients had noninvasive testing prior toangiography. The noninvasive testing regimenevolved over the 10-year period. For the past 6years, the routine noninvasive series has includedB-scan ultrasound imaging, direct Doppler(continuous-wave [CW] and pulse wave) examina-tion with spectral analysis, oculoplethysmography(OPG), and periorbital Doppler examination (PD).As we have previously reported, noninvasive stud-ies cannot reliably distinguish pseudo-occlusion fromocclusion of the ICA.9 Doppler-shifted ultrasoundtechniques measure the change that occurs when asignal of known frequency is reflected from a mov-ing target. When directed at the carotid artery, the

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O'Leary et al Pseudo-occlusion of ICA 1169

Doppler signal shift is proportional to the velocityof the erythrocytes within that part of the vessel.With increasing stenosis, erythrocyte velocity atthe point of maximal stenosis increases. However,with extreme degrees of stenosis, blood flow acrossthe stenosis decreases dramatically, with a corre-sponding fall in erythrocyte velocity. Doppler instru-ments contain high-pass filters to screen out low-amplitude echoes such as those generated by themovement of the carotid artery wall. When bloodflow is sufficiently low, the Doppler shift generatedby the movement of the erythrocytes will fall belowthis threshold and go undetected. Furthermore, thenumber of moving aggregates of erythrocytes in theICA may be too few to generate a signal of sufficientenergy to be distinguished from random back-ground noise. Thus, for both pseudo-occlusion andocclusion, the results of Doppler study will beidentical and will suggest the absence of blood flow.For both pseudo-occlusion and occlusion, B-scanultrasound imaging will demonstrate thrombus withinthe ICA and will suggest complete occlusion. Theresults of the indirect tests (OPG and PD) will besignificantly abnormal with both pseudo-occlusionand occlusion. Our noninvasive criteria for bothpseudo-occlusion and occlusion of the ICA were 1)absence of any frequency shift in the returningDoppler signal (no blood flow), 2) decrease of peaksystolic velocity in the ipsilateral common carotidartery compared with that of the opposite side, 3)ultrasonic visualization of a pattern of increasedechoes in the diseased ICA, 4) absence of pulsatilemotion, 5) abnormal OPG results on the side of thediseased vessel, and 6) reversal of blood flow in theipsilateral supratrochlear or supraorbital arteries.Our rationale for raising the possibility of pseudo-occlusion as opposed to complete occlusion afternoninvasive testing was basically clinical. If resultsof the noninvasive test suggested occlusion and ifsymptoms occurred within the month preceding thenoninvasive study and were appropriate to theabnormal vessel, pseudo-occlusion was suggested.

When pseudo-occlusion was suspected, theangiographic technique employed in 31 of the 34patients was that first described by Countee andVijayanathan.10 It was performed in the followingfashion: 1) selective catheterization of the com-mon carotid artery, 2) prolonged injection of high-dose contrast medium (4 ml Conray [Mallinckrodt,St. Louis, Missouri] 60/sec for 3-4 seconds, atotal of 12-16 ml), 3) filming in the lateral viewwith coning to include both the carotid bifurcationand the supraclinoid carotid artery, 4) prolongedfilming with 1 film/sec for 14 seconds, and 5)routine use of subtraction techniques. For the finalthree patients in this series, the angiographictechnique used was selective catheterization ofthe common carotid artery with digital subtractionangiography (DSA) (4 ml Conray 30/sec for 3seconds, a total of 12 ml; filming in the lateralprojection with 2 frames/sec for 14 seconds).

FIGURE 1. Right common carotid angiograms, lateralview, coned to include carotid bifurcation and supracli-noid carotid artery. Image at 12 seconds demonstratesthin trickle of contrast medium progressing cephalad tocavernous sinus (arrows).

The angiographic diagnosis of pseudo-occlusionwas made when a thin, markedly delayed antegradetrickle of contrast medium without discernible wash-out on later films was visible in the ICA distal to apoint of extreme stenosis (Figure 1). In most patientsthe contrast column had not reached the base of theskull by the 4-second film following injection.Patients presenting with high-grade stenosis butwithout layering or a significant delay in antegradeblood flow were not diagnosed as having pseudo-occlusion.

The decision to perform endarterectomy wasmade by the referring physician, based on thepatient's clinical presentation and associated riskfactors. No attempt was made to randomize patientswith respect to surgery. In practice, patients under-went endarterectomy unless there were specificcontraindications. Because most of these patientswere acutely symptomatic, management was car-ried out on an urgent basis. All patients scheduledfor surgery were heparinized immediately after angi-ography. Twenty-five patients had endarterectomy

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1170 Stroke Vol 20, No 9, September 1989

of the pseudo-occluded ICA performed by one ofeight surgeons, 21 patients within 24 hours and fourwithin 1 week after angiography. In no patient wasany unusual technical difficulty encountered at sur-gery. The other nine patients had medical treatmentof the pseudo-occlusion. Among the nine were twowho had a significant angiographic complication. Ofthe remaining seven, four still underwent surgery;three had endarterectomy of the opposite ICA for60-95% stenosis, and one was operated upon on theside of the suspected pseudo-occlusion but did notundergo endarterectomy after his surgeon decided,on direct inspection of the external surface of thevessel, that the ICA was not patent. The other threemedically treated patients were considered to beinoperable due to severe cardiac problems.

Periodic follow-up noninvasive studies to deter-mine vessel patency were performed after dis-charge. No patient had repeat angiography. At thetime of follow-up noninvasive testing, a history ofintervening neurologic symptoms was obtained. Clin-ical follow-up of patients was also accomplished bytelephone conversation with the patient, the family,and the primary physician.

ResultsResults of the initial noninvasive tests were sig-

nificantly abnormal in 33 of the 34 patients studied,occlusion or pseudo-occlusion in 31 and 75-99%stenosis in two. In one patient, results of thenoninvasive test were interpreted as normal. Thisoccurred in the first year, prior to the introductionof B-mode imaging and pulsed Doppler studies.

Five of the 34 patients had cerebral complicationsat angiography. Three of the five patients experi-enced TIAs in the territory of the pseudo-occludedartery; symptoms in two cleared within minuteswhile the third patient, whose deficit worsened overthe following 2 hours, underwent emergency endar-terectomy and was completely well following sur-gery. Two of the five patients had strokes on theside of the pseudo-occluded vessel, one duringangiography and one on the day after angiography.Neither patient underwent surgery, and both wereleft with significant neurologic deficits. To ensurethat this high incidence of complications did notreflect the overall complication rate for unselectedpatients, a control group of 195 consecutive patientswas taken for comparison. All 195 underwent carotidangiography for suspected extracranial carotid arterydisease between January 1983 and June 1984 andwere studied prospectively as part of anotherinvestigation.11 Except for an episode of transienthypotension, no angiographic complicationsoccurred in these 195 patients.

There were surgical complications in four patients.TIAs in two patients during the immediate postop-erative period resolved within a few hours. Twopatients experienced frank strokes. The first ofthese latter two patients had a history of stroke andprevious endarterectomy in the territory of the

pseudo-occluded vessel and presented with recur-rent TIAs. This patient had a total occlusion of thecontralateral ICA as well as bilateral vertebral arterystenosis and was left with mild hemiparesis. Thesecond patient was experiencing multiple TIAs andhad severe bilateral carotid artery disease. Thispatient had a stroke in the territory of the pseudo-occluded vessel at the time of surgery and died 2weeks later of myocardial infarction. Again, toensure that this complication rate was unique to thissubset of patients, a retrospective study of 191consecutive carotid endarterectomies done at ourhospital was taken for comparison. The retrospec-tive study demonstrated a perioperative stroke rateof 2.6% in diabetic patients and 0% in nondiabeticpatients.12

Patients were followed to determine vesselpatency and clinical outcome. Follow-up for vesselpatency in all nine patients treated medically showedocclusion. Two operated patients were lost to ves-sel patency follow-up. The average follow-up timefor the 23 remaining operated patients was 30 months(range 2 weeks to 73 months). Nineteen operatedpatients showed long-term patency of the previ-ously pseudo-occluded vessel, and four had totalocclusion. Thus, the patency rate following endar-terectomy was 83%.

Two of the 34 patients were lost to follow-up forclinical outcome. The average long-term follow-upfor clinical outcome among the 32 remaining patientswas 34 months (range 1 week to 73 months). Nooperated patient experienced delayed neurologiccomplications in the operated hemisphere. Twooperated patients did have contralateral strokes,one 6 months and one 24 months after surgery. Ofthe three medically treated patients who underwentendarterectomy of the opposite ICA, one had amajor stroke in that portion of the brain supplied bythe nonoperated pseudo-occluded vessel resultingin permanent neurologic disability 1 week followingsurgery. The second patient had a retinal arteryocclusion resulting in monocular blindness on thepseudo-occluded side 11 months after surgery. Thethird patient had no further neurologic symptoms.The medically treated patient who underwent explor-atory neck surgery but not endarterectomy had asevere stroke 3 months after surgery in the territoryof the pseudo-occluded vessel. The three medicallytreated patients for whom surgery was thought to becontraindicated because of cardiac risk factors expe-rienced no further neurologic deficits (Figure 2).

There were eight late deaths (average 16 months).Five occurred among the 23 operated patients andthree among the nine medically treated patients. Sixdeaths were from cardiac causes, and one each fromcancer of the lung and gastrointestinal bleeding.

DiscussionThe natural history of patients presenting with

pseudo-occlusion of the ICA is unknown. Pseudo-occlusion represents a moment late in the time

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O'Leary et al Pseudo-occlusion of ICA 1171

Ipsilateralstroke(2)"(at surgery)

Pseudo-occlusion

Endarterectomy^ (25)*

^ 1 \Contralateral No furtherstroke neurologic(2) events(6 mo, 24 mo) (19)

11 A\

\

No endarterectomy

//

Ipsilateralstroke(3)(1 wk, 3 mo,

11 mo)

(9) .

\ \Angiographic No furtherstroke neurologic(2) events

(4)

FIGURE 2. Flow diagramshowing clinical outcome of34 patients with pseudo-occlusion of internal carotidartery. The 25 patients repre-sented on the left underwentendarterectomy of pseudo-occluded artery. The ninepatients on the right did not,although three did undergocontralateral endarterectomy.*Two patients lost to follow-up; **one patient died at 2weeks after surgery.

course of a vessel progressing toward total occlu-sion. Significant blood flow to the brain is no longersupplied through pseudo-occluded vessels. If thepatient has not already experienced a debilitatingstroke, clinical concern focuses on the possibility ofa periocclusive embolus to the intracranial circula-tion or progressive thrombosis. Among our 34patients, 31 presented with either recent TIA orlocalized stroke in the territory of the pseudo-occluded vessel. These patients clearly represent apopulation at risk for further neurologic problems.Most authors believe that these patients requireaggressive management.1-10-13

Review of the literature reveals 62 reported casesof angiographically diagnosed atheromatous pseudo-occlusion of the ICA.1-10-13 Reports contain as manyas 13 and as few as one case. Fifty-six of these 62patients were symptomatic, and 54 had carotidendarterectomy. There were no reported complica-tions of either angiography or surgery, suggestingthat patients with pseudo-occlusion are at no par-ticular risk when subject to aggressive manage-ment. However, in our series four patients experi-enced significant strokes with permanent deficits,two related to angiography and two to surgery.Review of other series that relate the complicationrates of carotid endarterectomy to clinical presen-tation suggests that our experience is not unique.Sundt et al14 grouped patients according to preoper-ative evaluation of risk of carotid endarterectomy ina series that encompassed 342 operations. Neuro-logically stable patients without medical or angio-graphically determined risk factors (Group 1) had arisk for neurologic deficit at 1%. However, neuro-logically unstable patients (Group 4), into whichcategory almost all of our patients would fall, had a10% risk. Zurbrugg and his colleagues15 reviewed200 reports that encompassed 16,858 endarterecto-mies and found a mortality of 1.3% and a permanentmorbidity of 4.4% for patients presenting with TIAsand a mortality of 6.8% and a permanent morbidityof 10.2% for those presenting with stroke. Sincetheir papers deal only with the risk of surgery, ourcombined rate of mortality and permanent morbid-

ity for both angiography and surgery (12%) is notunexpected.

Our rate of serious complications would normallypreclude endarterectomy.16 However, a number ofstudies have suggested that symptomatic patientswith pseudo-occlusion or acute ICA occlusion areat increased risk for stroke.17-19 Certainly, the out-come in the seven medically treated patients havingno angiographic complication supports the impres-sion that these are patients at extremely high risk.Two of these seven had a major stroke and anotherlost vision in one eye, all appropriate to the side ofthe pseudo-occlusion.

There are at least four possible mechanisms ofstroke with pseudo-occlusive disease. These mech-anisms include hemodynamic ischemic insults, pro-gressive propagation of thrombus to the intracranialarteries, "stump" emboli passing through the exter-nal carotid circulation, and emboli arising from clotformed at the site of evolving occlusion, so-called"secondary emboli."20-24 Since pseudo-occludedvessels contribute little if any useful blood supply tothe cerebral hemisphere, ischemic infarction causedby a decrease in the critical blood flow seems to bean unlikely mechanism for injury. The usual atro-phic appearance of the cervical ICA distal to thesite of maximum stenosis supports this concept.The justification of endarterectomy then is largelyto prevent stroke from secondary emboli. All buttwo of our 34 patients were symptomatic, and, asdiscussed by Goldstone and Moore,25 the risk of notoperating in these circumstances may be quite high.It can be argued that the high rate of mortality andmorbidity associated with ICA occlusion may welljustify every attempt to prevent the periocclusivestate from progressing to the occlusive.26-28 Never-theless, we found the complication rates for angi-ography and endarterectomy in patients with ICApseudo-occlusion to be high and possibly to out-weigh any benefit derived from surgery.

The patency rate among the 23 operated patientswho were followed up was 83%. Of the four forwhom the attempt to reopen their vessel failed,none suffered any postoperative complication. Allfour were found to have abnormal noninvasive test

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1172 Stroke Vol 20, No 9, September 1989

results immediately following endarterectomy. Noneof the 19 with normal noninvasive test resultsimmediately after surgery later occluded, nor didthey experience any further neurologic deficit onthe operated side. Two of the 19 patients whounderwent successful endarterectomy later suffereda stroke in the opposite circulation, emphasizing theseverity of the atherosclerotic process in this group.

Ringelstein et al13 described nine patients in whomthe diagnosis of pseudo-occlusion was made pro-spectively with CW Doppler. These authors recom-mended careful examination of the region of thecarotid bulb to detect a faint, sharp, and continuoushissing sound. This tone was stated to be charac-teristic of pseudo-occlusion. Our examination pro-cedure with CW Doppler appears to parallel theirs,but we identified this finding in only two of our 34patients. If we had depended upon the detection ofa faint, nonpulsatile hiss detected with CW Dopp-ler, we would have overlooked the diagnosis ofpseudo-occlusion in 94% of our patients. Rushtonand Kukora19 reported findings similar to ours andconcluded that noninvasive tests could not reliablydistinguish very-high-grade stenosis from total occlu-sion. This observation is important since the non-invasive findings may determine how aggressivelythe diagnosis of pseudo-occlusion is pursued atangiography.

While selective carotid angiography with injec-tion of medium high-dose contrast and prolongedfilming was critical to the diagnosis of pseudo-occlusion, the possible contribution of angiographyto the high complication rate we experienced can-not be overlooked. Injection of a large volume ofcontrast medium under pressure immediately prox-imal to fresh thrombus may well pose a significanthazard. As previously noted, no similar problemswere reported by other authors. In 1984, wedecreased our injected volume from 16 to 12 ml. Ithas been suggested that rapid-sequence axial com-puted tomography (CT)29 and intravenous DSA30

could be used to diagnose pseudo-occlusion withoutrisk to the patient. We have no experience with theformer and have been disappointed in our limitedexperience with the latter. Limited resolution, patientmovement, misregistration artifacts, superimposi-tion of vessels, and the inability to obtain a lateralview all pose significant problems in the use ofintravenous DSA. Intra-arterial DSA, with selec-tive injections of smaller volumes of contrastmedium, should be able to replace high-dose delayedconventional angiography in patients with pseudo-occlusion, possibly lowering the incidence of angio-graphic complications. We studied our last threepatients using only selective intra-arterial DSA,achieving good-quality studies without any adversereactions.

Our retrospective study suggests that aggressivemanagement of atheromatous pseudo-occlusion ofthe ICA carries a significantly worse prognosis thanthat reported by other authors. Of the 34 patients

with pseudo-occlusion undergoing angiography, five(15%) had angiographically related ischemic symp-toms. Of the 25 patients having endarterectomy,four (16%) experienced ischemic symptoms. Amongour 34 patients with pseudo-occlusion, four (12%)were left with fixed neurologic deficits, two relatedto angiography and two to surgery. Unfortunately,the outcome for patients not undergoing surgeryappears correspondingly bleak. Excluding the twopatients who suffered irreversible ischemic deficitsat the time of angiography, three of the sevenmedically treated patients later experienced signif-icant deficits in the territory supplied by the pseudo-occluded vessel. None of these medically treatedpatients was heparinized.

Our study does demonstrate four facts: 1) pseudo-occlusion is a very unstable situation; 2) angiogra-phy and surgery represent a significant risk forpatients with pseudo-occlusion; 3) endarterectomyis technically feasible, long-term patency of theoperated vessel is high, and distant neurologicsequelae within the territory supplied by the oper-ated vessel are rare; and 4) the major long-term riskfor these patients is cardiac disease. The highcomplication rate of angiography and surgery mustcause us to reflect on the proper management ofthese patients. We conclude that surgical interven-tion remains appropriate in part because the long-term outcome for patients successfully operatedupon was good and in part because the suspectedoutcome in patients treated conservatively wouldnot be as good. We recognize that we do not haveadequate data to support this latter supposition.When surgery is contemplated, certain steps shouldbe taken to lower the incidence of complications.The volume of contrast medium used at angiogra-phy should be reduced. DSA should be employedwhenever pseudo-occlusion is suspected. In ourmost recent case of suspected pseudo-occlusion,which proved at angiography to be occlusion, weused only 6 ml Conray 30. Whether the use ofintra-arterial DSA and small volumes of contrastmedium are always adequate in this setting remainsto be proven, but it seems reasonable to start theexamination in this fashion. Additional injectionswith cut film can always be performed if necessary.Also, more attention needs to be focused on theneurologic status of these patients at the time ofpresentation. Management should be based on this,rather than on results of angiographic study. It is asurgical axiom that thrombus is best removed whilestill fresh. If patients are neurologically stable, orhave had a neurologic deficit that has cleared, andthe history and results of noninvasive tests suggestpossible pseudo-occlusion, we recommend emer-gency angiography and endarterectomy. In patientswith fluctuating or small "fixed" neurologic defi-cits, we would perform a CT or magnetic resonanceimaging scan as the first step. If this shows no lesionor a small lesion, we would handle them as asymp-tomatic patients. In patients who present with a

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O'Leary et al Pseudo-occlusion of ICA 1173

significant or progressing neurologic deficit, wesuggest that angiography and surgery be delayeduntil the patient is in stable condition. During thewaiting period emboli should be prevented by anti-coagulation, first with heparin and later, if neces-sary, with warfarin. Buchan and his colleagues31

suggested such an approach in the management ofpatients who presented with intraluminal thrombusin the carotid arteries because of the significantrisks they found associated with emergency endar-terectomy. Other authors recommend the sametreatment for neurologically symptomatic patientswith tight carotid stenosis.32'33 While it is unlikely tooccur, to truly answer the question whether this isadequate therapy for pseudo-occlusion would requirea prospective randomized study.

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KEY WORDS • angiography • carotid artery disease •cerebrovascular disorders

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D H O'Leary, H Mattle and J E PotterAtheromatous pseudo-occlusion of the internal carotid artery.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1989 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.20.9.1168

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