Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_5776_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

30.08.2026

Размер:

53 Мб

Скачать

☆

<<< < Предыдущая 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 4344 / 5044 45 46 47 48 49 50 > Следующая >>>

Case 28

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to Extracranial–Intracranial Bypass Surgery

409

Clinical Presentation

A 50-year-old woman was admitted to the emergency department with acute weakness of her left arm, left drooping lip, and slurred speech. She had woken up with these symptoms that morning. One year previously, she had had two transient episodes of left-sided hemihypesthesia, each lasting about 20 minutes. She had multiple vascular risk factors including arterial hypertension, h y p e r c h o l e s t e r o l e m i a , a n d h e a v y s m o k i n g . O n a d m i s sion, the neurologic examination revealed left-sided supranuclear facial palsy, mild left-sided sensorimotor hemiparesis, and dysarthria (National Institute of Health Stroke Scale [NIHSS] score: 6).

Initial Neuroradiologic Findings

Cranial CT demonstrated early signs of extended rightsided territorial middle cerebral artery (MCA) infarction, which was conﬁ rmed by MRI. Time-of-ﬂ ight MR angiography (TOF-MRA) depicted absent signals of the right internal carotid artery (ICA) and right MCA and a prominent right posterior communicating artery (PCoA) (Fig. B28.1 and Fig. B28.2).

Suspected Diagnosis

Ischemic right-sided MCA infarction in ICA and M1-MCA occlusion. Thrombolysis was not performed because the unknown time of stroke onset (wake-up stroke) and because of the CT ﬁ ndings visualizing ischemia in more than one-third of the MCA territory.

Questions to Answer by Ultrasound Techniques

• Was there evidence of atherosclerotic change in the extracranial brain-supplying arteries?

• Was there a sustained occlusion of the right ICA and MCA? If so, was there evidence of collateral blood ﬂ ow via the anterior (ACA) and posterior (PCA) cerebral arteries or the ophthalmic artery (OA)?

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode imaging revealed severe atherosclerotic changes in extracranial vessels with distinct accentuation in the right carotid bifurcation. A high-resistance ﬂ ow signal with reduced ﬂ ow velocity and increased pulsatility was seen in the right common carotid artery (CCA). The right external carotid artery (ECA) was normal. No ﬂ ow signal was seen in the right ICA. Both vertebral arteries (VAs) were of normal caliber in the V2 segment (left, 4.1 mm; right, 3.9 mm). Flow assessment of the left VA demonstrated an almost retrograde ﬂ ow with only a minimal diastolic ﬂ ow component. Upper arm compression test with a blood pressure cuﬀ (pressure above the systolic blood pressure) led to a bidirectional ﬂ ow signal with ret- rograde systolic and antegrade diastolic ﬂ ow component. Release of the pressure cuﬀ (reactive hyperemia of the arm) led to completely retrograde ﬂ ow. Increased ﬂ ow velocities but otherwise normal ﬂ ow signals were seen in all detectable segments of the right VA. Both V0-VA segments and the subclavian arteries (SAs) could not be visualized (Figs. B28.3–B28.9; see also Video

Transcranial Duplex Sonography

The right M1-MCA and A1-ACA segments revealed an obvious poststenotic ﬂ ow pattern with antegrade A1- ACA ﬂ ow. A positive oscillation eﬀ ect in the right MCA was seen during slight tapping of the right VA at the level of the atlas loop. Marked turbulence including a musical murmur was observed in the right PCoA at its junction with the PCA. On the left side a strong antegrade A1-ACA segment was seen (ﬂ ow velocity 142/74 cm/s). The anterior communicating artery (ACoA) was not visible. The left M1-MCA segment was normal (ﬂ ow velocity 110/60 cm/s). The right P1-PCA had a markedly increased ﬂ ow velocity (160/100 cm/s). Both P2- and P3-PCA segments had ﬂ ow velocities at normal ranges with a post- stenotic ﬂ ow pattern. Transforaminal insonation revealed a nearly complete retrograde systolic ﬂ ow component in the left V4-VA segment similar to the extracranial

B28.1).

410 Case 28 Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to

Extracranial–Intracranial Bypass Surgery

ﬁ ndings and a normal antegrade ﬂ ow in the right V4-VA segment. The basilar artery (BA) showed a poststenotic ﬂ ow pattern. On transorbital insonation, the right OA could not be seen (Fig. B28.10–B28.19; see also Video

B28.2).

Cerebrovascular Reactivity Testing

Intravenous administration of 1 g acetazolamide induced a 31% increase of mean ﬂ ow velocity above baseline lev- els in the left M1-MCA and an 8% decrease in the right M1-MCA, indicative of a steal phenomenon (Fig. B28.20).

Conclusion

Severe atherosclerotic vascular changes with proximal occlusion of the right extracranial ICA but with a patent right MCA. Insuﬃ cient intracranial collateral blood ﬂ ow toward the right MCA and ACA via the right PCoA. Additional collateral ﬂ ow toward the right ACA via the left ACA (double ﬁ lling). Furthermore, indirect signs of left proximal SA occlusion or high-grade stenosis with asymptomatic subclavian steal phenomenon grade III. Notably, the right VA was the only patent vessel providing blood ﬂ ow, not only to the total posterior circu- lation but also to the right anterior circulation and to the left arm.

Conventional Angiography (Day 2)

Digital subtraction angiography (DSA) conﬁ rmed the prox- imal occlusion of the right ICA and the collateralization of the right MCA territory via the right PCoA. On selective left ICA injection, double ﬁ lling of both A2-ACA segments via the left A1-ACA segment was observed. In addition, a left SA occlusion was detected and the subclavian steal phenomenon was conﬁ rmed (Figs. B28.21–B28.26).

Clinical Course (1)

A periocclusional embolism on the basis of severe atherosclerosis originating from the right ICA with spontaneous recanalization was thought to be the cause of the MCA infarction. Subsequently, long-term secondary stroke prevention was started with aspirin. Because of the impaired intracranial collateralization, mildly hypertensive blood pressure values were tolerated. A right EC–IC bypass was discussed but the decision was postponed until re-examination of cerebrovascular reactivity (CVR) and evaluation of the clinical course 4 weeks later. During the hospital stay, the left-sided hemiparesis improved markedly.

Follow-up Neurosonologic Findings (4 Weeks)

Extracranial Duplex Sonography

Assessment of the extracranial arteries remained unchanged demonstrating the right-sided ICA occlusion and left-sided subclavian steal phenomenon (not shown).

Transcranial Duplex Sonography

Unchanged intracranial ﬁ ndings (not shown).

Cerebrovascular Reactivity Testing

A 52% acetazolamide induced ﬂ ow increase was seen in the left M1-MCA. The right M1-MCA demonstrated a 16% ﬂ ow decrease (not shown).

Conclusion

Right extracranial ICA occlusion with unchanged intracranial collateralization mainly via the right PCoA. Unchanged asymptomatic subclavian steal phenomenon grade III on the left side. Worsened CVR implicating an increased risk of developing hemodynamic ischemia.

Fig. B28.27 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

Clinical Course (2)

A right-sided STeA–MCA bypass was performed. The intervention was uneventful and the angiographic control immediately after surgery showed a patent collateral vessel (not shown). CT revealed no intracranial bleeding and no new ischemic brain damage. Longterm stroke prevention with clopidogrel was recommended. Follow-up over a 4-year period revealed no further ischemic events.

Final Diagnosis

Periocclusional right territorial MCA infarction caused by an occlusion of the right ICA. Impaired intracranial collateralization with cross-ﬂ ow via the ACoA only to the con- tralateral ACA territory and insuﬃ cient collateral ﬂ ow to the MCA via the ipsilateral PCoA, complicated by a left subclavian steal phenomenon. Successful insertion of an STeA–MCA bypass on the right side.

Fig. B28.1 Cerebral MR T2-weighted image, axial plane. Right par-

tial territorial MCA infarction sparing the basal ganglia.

Final Diagnosis

Fig. B28.2 3D TOF-MRA, axial maximal intensity projection (MIP). Absent right ICA signal and large signal gap in the course of the right MCA (arrows) suggestive of distal M1-MCA and ICA occlusion. Note the prominent distal ICA perfused by the right PCoA (arrowhead).

411

CCA-L

Fig. B28.3 Extracranial duplex, longitudinal plane. Normal left CCA

ﬂ ow (ﬂ ow velocity 76/35 cm/s, PI = 1.25).

CCA-R

Fig. B28.4 Extracranial duplex, longitudinal plane. Resistance ﬂ ow signal with reduced velocity and increased pulsatility in the right CCA (ﬂ ow velocity 33/15 cm/s, PI = 1.39).

412 Case 28 Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to

Extracranial–Intracranial Bypass Surgery

ICA-R

Fig. B28.5 Extracranial duplex, longitudinal plane. Absent signal in the right ICA.

V2-VA-R

V2-VA-L

Fig. B28.6 Extracranial duplex, longitudinal plane. Retrograde systolic ﬂ ow with at best minimal antegrade diastolic ﬂ ow in the normal- ly developed left V2-VA (diameter 4.1 mm, ﬂ ow velocity 84/0 cm/s).

V2-VA-L

Fig. B28.7 Extracranial duplex, longitudinal plane. Increased antegrade ﬂ ow in the normally developed right V2-VA (diameter

3.9 mm, ﬂ ow velocity 160/88 cm/s).

V2-VA-L

Cuff release

Fig. B28.9 Extracranial duplex, longitudinal plane. Left V2-VA after the release of upper arm compression (arrow) leading to reactive hyperemia and completely retrograde ﬂ ow.

Cuff pressure >

systolic blood pressure

Fig. B28.8 Extracranial duplex, longitudinal plane. Left V2-VA during upper arm compression, induced by a blood pressure cuﬀ inﬂ at- ed to more than the systolic blood pressure (arrow), leading to a bidirectional ﬂ ow signal with antegrade diastolic ﬂ ow.

M1-MCA-L

Fig. B28.10 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Almost normal ﬂ ow signal in the left M1-MCA (ﬂ ow velocity 110/60 cm/s).

Final Diagnosis

413

M1-MCA-R

Fig. B28.11 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Distinct poststenotic ﬂ ow pattern in the right M1-MCA (ﬂ ow velocity 55/35 cm/s).

A1-ACA-R

A1-ACA-L

Fig. B28.12 TCC S (t rans tempo ral ap proa ch), l eft- sided insonation, midbrain plane. Marked but otherwise normal ﬂ ow in the left A1-ACA indicating collateral ﬂ ow (ﬂ ow velocity 142/74 cm/s).

PCoA-R

Fig. B28.13 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Antegrade ﬂ ow with a poststenotic ﬂ ow pattern in the right A1-ACA identical to the pattern of the right M1-MCA (ﬂ ow velocity 52/33 cm/s).

P1-PCA-R

Fig. B28.15 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Turbulent ﬂ ow with increased ﬂ ow velocity in the right P1-PCA indicating collateral ﬂ ow via PCoA (ﬂ ow velocity 160/100 cm/s).

Fig. B28.14 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Musical murmurs in the right PCoA at the junction with the PCA indicating functional stenosis.

P2-PCA-R

Fig. B28.16 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Marked poststenotic ﬂ ow pattern in the right distal P2-PCA with otherwise normal ﬂ ow velocities (40/30 cm/s).

414 Case 28 Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to

Extracranial–Intracranial Bypass Surgery

P2-PCA-L

Fig. B28.17 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , thalamic plane. Poststenotic ﬂ ow pattern in the left distal P2-PCA (ﬂ ow velocity 75/50 cm/s).

V4-VA-R

V4-VA-L

Fig. B28.18 TCCS (t rans foram inal app roach). Alm ost re trograde

ﬂ ow in the left V4-VA similar to the ﬂ ow signal in the left V2-VA (ﬂ ow velocity 80/−2 cm/s).

Velo city (cm/s )

150

MCA-L + 31%

100

Fig. B28.19 TCC S ( transfo rami nal app roac h). Pro mine nt but otherwise normal ﬂ ow signal in the right V4-VA (ﬂ ow velocity 90/35 cm/s).

MCA-R

13:55

14:00 14:05 14:10

- 8%

Time (min)

Fig. B28.20 Acetazolamide infusion test, bilateral TCD monitoring of M1-MCA ﬂ ow velocity. Marked diﬀ erence between the right and left sides with an increase in ﬂ ow velocity of 31% on the left and a decrease of 8% on the right side (steal phenomenon).

Fig. B28.21 DSA, right CCA injection, lateral view. Proximal occlusion of the right ICA (arrow).

Fig. B28.22 DSA, left CCA injection, posteroanterior view. Normal left-sided intracranial anterior circulation. Filling of the right ACA territory via the left A1-ACA (arrows).

415Discussion

Fig. B28.23 DSA, right VA injection, posteroanterior view. Filling of the right MCA vessels (arrows) via the right PCoA (arrowhead). Note the absent ﬁ lling of the ACA.

Fig. B28.25 DSA, brachiocephalic angiogram, left anterior oblique (LAO) view. Proximal left SA occlusion (arrow).

Fig. B28.24 DSA, right VA injection, lateral view. Note the prominent right PCoA (arrow).

Fig. B28.26 DSA, right VA injection, lateral view, late arterial phase. Note the retrograde left VA ﬁ lling (arrows) and the distal SA ﬁ lling (arrowhead) following contralateral VA contrast injection.

Discussion

Clinical Aspects

2010, Wouters et al 2014). WUS is a major obstacle for thrombolysis. Comparable to myocardial infarction and sudden cardiac arrest, a diurnal variation in the onset

of stroke with predominance in the morning and even Our 50-year-old patient had woken up with ischemic symptoms of MCA stroke. On cranial CT early signs of extended right-sided MCA infarction were detected and therefore no thrombolysis was performed. Unknown time of onset including so-called wake-up stroke (WUS) is observed in ~20–25% of patients (Silva et al

just prior to awakening is well known but not well un-

derstood. Endogenous factors like an increase in blood

pressure or in platelet aggregation may be contributing

factors (Kario et al 2011). To explore the possibility of

oﬀ ering patients thrombolytic therapy in WUS, a large

European multicenter trial (WAKE-UP) is currently

416 Case 28 Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to

Extracranial–Intracranial Bypass Surgery

functional ACoA via the contralateral A1-ACA. Second, the MCA is in most cases the extension of the ICA whereas the origin of the ACA has an unfavorable angle and is therefore not the preferential route of emboli. Last, a major ﬂ ow is usually present in the MCA, which favors the receipt of emboli. It has been shown that in patients with isolated territorial infarctions of the ACA, this vessel had a larger diameter than the ipsilateral M1-MCA, which supports this assumption (Shoamanesh et al 2014).

It has been assumed that ~15% of large embolic artery infarctions are caused by acute ICA occlusions. The underlying mechanism of periocclusional embolism might be a critical slowing of blood ﬂ ow within a stenosis. This then leads to embolus formation which in the moment of ICA occlusion detaches, and leads to intracranial vessel occlusion and in-

farction. Embolism may, however, rarely also occur after completed vessel occlusion from the distal “tail” of a propagating carotid thrombus (Finklestein et al 1980). More theo-

Fig. B28.27 Schematic of the patient’s extra- and intracranial brain-supplying arteries before EC–IC bypass. Right proximal ICA occlusion and left proximal SA occlusion (circles). Collateralization of the right MCA territory through the right VA via BA and right PCoA. Collateralization of the right ACA territory in part through the left ACA. Blood supply to the left distal SA via retrograde left VA fro m th e r ight VA (arr ows ). Not e t hat th e r igh t VA pr ovi des th e blood ﬂ ow for the total posterior circulation, right MCA territory, part of the right ACA territory and left arm.

retically, the proximal stump of the occluded ICA may be the source of emboli, for example, if an ICA embolus originating from the stump follows the collateral pathways via the ECA and retrograde OA into the brain. MCA embolism may also occur in ICA occlusion primarily as an artery-to-artery event in CCA and ECA plaque lesions (Barnett et al 1978).

Hemodynamic compromise is the second common cause of ischemia in ICA occlusions (Pessin et al 1979). In cases with insuﬃ cient collateral blood supply, reduced per- fusion in the border zones between the vascular territories

analyzing the relationship of signal increases in diffusion-weighted (DW) and ﬂ uid-attenuated inversion recovery (FLAIR)-weighted images (diﬀ usion–FLAIR mismatch) on MRI. The hypothesis is that hyperacute ischemia will show DWI lesions but no corresponding FLAIR correlates, which would then allow thrombolysis in strokes of unknown onset (Thomalla et al 2014).

Our patient had severe atherosclerosis of the

brain-supplying arteries, associated with multiple vascular risk factors including smoking. She suﬀ ered from a right MCA infarction, most probably caused by a “ﬁ nal” periocclusional artery-to-artery embolism in ICA occlusion. An asymptomatic left subclavian steal phenomenon (SSP) on the basis of a left proximal SA occlusion was also detected. Both pathologies resulted in a complex extraand intracranial hemodynamic situation. Because of the good regression of neurologic deﬁ cits, the patient’s rel- atively young age, and the exhausted CVR, an STeA–MCA bypass operation was performed to improve the perfusion of the right hemisphere. In the following discussion we ﬁ rst address the implications of ICA occlusion and then those of the SSP.

The incidence of symptomatic unilateral ICA occlu-

sions is 6/100,000 (Flaherty et al 2004). Considering that not every patient suﬀ ering a transient ischemic attack (TIA) consults a doctor, the number may even be higher. The incidence of asymptomatic ICA occlusions is unknown. In symptomatic cases cerebral or retinal ischemia may be hemodynamic or, more often, embolic in nature. Embolism may result in acute carotid-T occlusion which, however, most frequently leads to an involvement of the MCA territory, less frequently of the ACA territory or of both territories combined. The dominance of MCA territorial infarctions is explained by three aspects. First, an A1-ACA occlusion can be compensated in the presence of a

may result in hemodynamic infarctions (BZI). This assumption is supported by an obvious association of BZI and ICA occlusions or high-grade stenoses (Baumgartner and Regard 1994, Hupperts et al 1996, Weiller et al 1991) (for further discussion on BZI, see also Chapter 4, “Border Zone Infarction” under “Classiﬁ cation of Arterial Stroke,” and Case 30).

Hemodynamic TIAs may present with speciﬁ c pat- terns. Often, TIAs occur with cortical signs, for example, in relation to orthostatic hypotension (Caplan and Sergay 1976, Ruﬀ et al 1981, Somerville 1984). Occasional- ly “limb shaking” may be observed (Nguyen et al 2011, Persoon et al 2010). This phenomenon, ﬁ rst described in 1962 by Fisher, comprises unilateral repetitive involuntary movements of arm and/or legs without epileptic activity on electroencephalogram (EEG) analysis. The detailed mechanism of this phenomenon is not well understood; however, it ceases after successful carotid endarterectomy (CEA) or an EC–IC bypass (Baquis et al 1985, Tatemichi et al 1990, Yanagihara et al 1985). In contrast to amaurosis fugax, usually associated with extracranial ICA stenoses and indicative of artery-to-artery embolism, a transient retinal ischemia or “retinal claudication” is a less well known symptom. Looking into bright light increases the retinal metabolic demand. In combination with the already impaired retinal perfusion in patients with an ICA occlusion, this may subsequently manifest by diminished visual acuity after visual stimuli (Furlan et al 1979). Chronically reduced orbital blood ﬂ ow may lead to venous stasis retinopathy, which is often clinically asymptomatic and may be diagnosed by ophthalmoscopy. In patients with ICA occlusion a venous stasis retinopathy was observed in 32 of 110 patients (29%). Clinically manifest chronic ocular ischemia is rare, with a published annual rate of 1.5% (Klijn et al 2002). For further reading on amaurosis and central artery occlusion, see Case 38).

417Discussion

The two ischemic mechanisms, embolic and hemodynamic, may facilitate each other. Animal experiments have demonstrated that the extent of embolic infarctions rises in cases with generally impaired cerebral hemodynamics, probably as a result of insuﬃ cient and delayed disruption of emboli (Omae et al 2000).

The functioning of the available collaterals determining the degree of impairment in cerebral hemodynamics can be assessed by several diagnostic methods, such as PET, SPECT, MRI, and transcranial ultrasound. A measure of collateral function is the CVR which can easily be determined by transcranial Doppler (TCD) (see also Chapter 3, “Metabolic Coupling”). Applying this method to patients with an ICA occlusion, ~12% of cases demonstrate an exhausted CVR and 29% an impaired CVR (Widder et al 1994). The former was especially seen in patients who had experienced cerebral ischemia in the 3 months prior to the analysis. In cases with acute occlusion, the CVR undergoes constant changes as collateral function may improve over time. Therefore, CVR improves over time too and may not be stable before 3–4 weeks post ischemia. The assumption that CVR normalization occurs over several months was not conﬁ rmed, however (Rutgers et al 2000). In our patient, we repeated CVR testing after 4 weeks, which demonstrated further progression of the hemodynamic failure.

Patients with asymptomatic ICA occlusions have a good long-term prognosis. A case series in 30 patients reported only one ischemic stroke during an observational period of 32 months (Powers et al 2000). An analysis of symptomatic patients from 20 clinical studies, who had suﬀ ered a retinal TIA, cerebral TIA, or minor stroke, re- vealed a general annual risk of stroke of 5.5% and a risk of an ipsilateral stroke of 2.1%. Patients with impaired CVR had an even higher annual risk of 12.5% for general stroke and of 9.5% for ipsilateral stroke, both substantially higher than for the total group of ICA occlusions. Patients with an exhausted CVR had the highest risk, with 41.4% for general stroke and 31% for ipsilateral stroke, respectively (Klijn et al 1997).

Secondary stroke prevention in ICA occlusion is mainly achieved by antiplatelet medication. In cases of acute ICA occlusion, anticoagulation therapy is sometimes given for several weeks to prevent embolic events from the stump. However, there are no data from controlled trial to support this approach.

Another therapeutic aspect is blood pressure management. Large epidemiologic studies have shown that blood pressure reduction leads to subsequent reduction of stroke risk. However, in patients with impaired hemodynamics due to severe steno-occlusive disorder normal blood pressure might be a risk factor for hemodynamic cerebral ischemia. In these cases, moderately elevated blood pressure values might be tolerated or an intervention (such as CEA or stenting of an ipsilateral asymptomatic high-grade stenosis in case of contralateral ICA occlusion) considered. In cases of unilateral chronic ICA occlusion, a deliberate increase of blood pressure is not recommended as it does not reduce the risk of future strokes but increases the risk of cardiac events (Rothwell et al 2003c).

Interventional revascularization approaches such as the insertion of an EC–IC bypass are controversial, but

have been largely abandoned since publication of the EC–IC Bypass Study results in 1985. In this trial, which included patients with symptomatic high-grade ICA or MCA stenosis or occlusion, no beneﬁ t was found for pa- tients who had been operated on compared with those who had best medical treatment (EC/IC Bypass Study Group 1985). For further reading on EC–IC bypass treatment, see also Case 25 and Case 9.

In addition to the ICA occlusion, our patient presented an occlusion of the left proximal SA and a subsequent SSP. A SSP is deﬁ ned as the reversal of blood ﬂ ow in a VA, ipsilateral to an upstream proximal high-grade SA stenosis or occlusion. The left side is mostly aﬀ ected in a ratio of ~4:1 which is usually explained by the acute angle of origin of the left SA, which increases ﬂ ow turbulence and accelerates atheroscle- rosis (Labropoulos et al 2010, Nicholls et al 1991). The VA then takes over the insuﬃ cient blood supply of the ipsilat- eral arm. Fisher named the phenomenon “subclavian steal” in 1961 as the ischemic arm “steals” blood from the intracranial circulation. The reported prevalence of the SSP is between 1.9% (in a population-based analysis of blood pressure diﬀ erences >15%) and 9% (in patients with a neck bruit) (Bornstein and Norris 1986, English et al 2001, Shadman et al 2004). Atherosclerotic occlusive disorders of the SA correlate with past and current smoking history, hypertension, and especially with the presence of a peripheral arterial occlusive disease (PAOD). An angiographic study reported prevalence for SA stenosis of 4.3% in patients who smoked,

6.8% in patients with diabetes mellitus, 7.6% in patients with cerebrovascular events, and 11.5% in patients with PAOD (English et al 2001). Besides atherosclerosis, other causes such as congenital deformities, traumatic injuries, radiation emboli, or inﬂ ammatory diseases like giant cell arteritis and in particular Takayasu’s arteritis, might lead to the SSP (see also Case 23). Depending on the anatomic vessel course, SA stenoses or occlusions with subsequent SSP occur in twothirds of cases on the left side and in one-third of cases on the right (Kaneko et al 1998, Tan et al 2006). Rarely a SSP may be present bilaterally (Budincevic et al 2014).

Whenever transient or persisting clinical symptoms are observed, the term subclavian steal syndrome is used instead of SSP. A variety of symptoms may occur including headaches, episodes of transient brainstem ischemia, activity-related pain (arm claudication), and sensory disturbances as well as impaired strength in the aﬀ ected arm. Headaches, particularly located in the neck, or the mastoid or occipital regions, which may be ampliﬁ ed by physical activity, are frequently reported in subclavian steal syndrome. Resting and exertional arm pain or other impairments of the arm are rather infrequent ﬁ ndings. This might be explained by the slow progression of the SA occlusive disorder with the subsequent development of other additional collateral pathways. TIAs are often short, lasting only seconds to minutes. The symptoms may be diﬃ cult to recognize as they often only become obvious if there are additional occlusions in the anterior circulation or there is inadequate collateralization. A large study including 324 patients with a subclavian steal found symptoms related to an impaired perfusion of the posterior circulation in only 5% of cases. In contrast, 31% had, as in our case, symptoms attributable to the anterior circulation

418 Case 28 Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to

Extracranial–Intracranial Bypass Surgery

because of a generalized severe atherosclerosis also aﬀ ecting the carotid arteries. The remaining 64% of pa- tients were asymptomatic (Hennerici et al 1988). When considering therapeutic measures, the often complex vascular constellation has to be taken into consideration. Until the 1980s, patients with a subclavian steal were often treated by vascular surgery even if they were asymptomatic. Today these procedures are considered only in symptomatic patients and after critical evaluation of the complete hemodynamic situation. In most cases, however, no intervention is required (for further discussion on therapeutic aspects, see also Case 23).

Angiologic and Anatomic Aspects

The SSP is characterized by a reversal of ﬂ ow within the aﬀ ected VA, illustrating the compensatory ability of the cerebral circulation. Determined by the degree of stenosis of the SA, three grades of SSP can be diﬀ erentiated (Thomassen and Aarli 1994):

• Grade 1—incipient SSP: This grade is characterized by a gradual diminution of systolic VA ﬂ ow but preserved diastolic ﬂ ow, called systolic deceleration. This depres- sion in ﬂ ow velocity reﬂ ects a loss of VA perfusion pres- sure during the highest ﬂ ow velocity in the SA (Kliewer et al 2000).

• Grade 2—incomplete SSP: This grade is characterized by a pressure adjustment leading to a biphasic alternating ﬂ ow signal with a retrograde systolic and an ante- grade diastolic ﬂ ow component.

• Grade 3—complete SSP: This is characterized by a complete ﬂ ow reversal, observable in all segments of the aﬀ ected VA, which usually occurs in complete SA occlusion.

The same monophasic VA ﬂ ow proﬁ le can then also be observed in the dependent distal arteries (e.g., the brachial artery), which allows a fast indirect evaluation of SA pathology. The described ﬂ ow patterns apply to the patient at rest. Muscular activity within the aﬀ ected arm leading to reactive hyperperfusion will alter the observed VA ﬂ ow proﬁ les. This principle may also be applied as a controlled test for an SSP. A blood pressure cuﬀ posi- tioned on the aﬀ ected arm is inﬂ ated above systolic blood pressure levels under continuous monitoring of the VA ﬂ ow. During this phase of arm ischemia the VA ﬂ ow may improve or normalize. On sudden release of the pressure cuﬀ the arm becomes hyperemic and the VA ﬂ ow abnor- mality worsens, usually by one grade. Such a change was observed in our patient. The description of ﬁ ndings in the ultrasound report should therefore include the SSP grade at rest and under provocation unless grade 3 SSP is already present at rest.

Ultrasound diagnosis of the SSP is easy because the combination of extracranial duplex and transcranial color-coded duplex sonography (TCCS) permits a clear description of ﬂ ow pathology within the extracranial and intracranial VAs and the BA. In patients with a grade 2 or 3 SSP the diagnosis is straightforward. More diﬃ cult may be the diﬀ erentiation of grade 1 SSP from a mild- ly poststenotic ﬂ ow, caused by a proximal VA stenosis,

which might not be accessible to ultrasound diagnostics. In these cases the above blood pressure cuﬀ test and ﬂ ow signal assessment of the distant VA or BA will be of help as no relevant modulation of the ﬂ ow proﬁ le is to be ex- pected in the case of proximal VA stenosis.

ther hemodynamic eﬀ

Ano

ect of SSP on the posterior

circulation is the increased ﬂ ow in the nonaﬀ ected VA, which occurs in all cases with a vertebro-vertebral overﬂ ow. As may be expected, this eﬀ ect will be greater in grade 3 than in grade 2 SSP (Tan et al 2006). Furthermore, the SSP may additionally provoke a basilar steal phenomenon. An incomplete basilar steal comprising a systolic ﬂ ow deceleration at rest was seen in 7 of 55 patients with SSP, increasing to 25 if additional provocation tests were performed. A complete basilar steal phenomenon, however, is rare. It was found at rest only in one patient in this study. A basilar steal was present in seven of eight cases with deﬁ nitive symptoms of posterior circulation and in ﬁ ve of six symptomatic patients with a >50% contralateral VA st en os is , i ndic at in g t hat pa ti en ts wi th a b as il ar stea l are at higher risk of stroke (de Bray et al 1994).

Our case presented a pathologic poststenotic ﬂ ow pat- tern, not only in the BA but also in both PCAs without the presence of a proximal VA or BA stenosis. This ﬂ ow altera- tion can therefore be explained by the proximal SA occlusion and by a lack of collateral blood ﬂ ow from the anterior circulation due to an additional extracranial ICA occlusion. At least the nonaﬀ ected right VA assured the blood supply of the left arm, the brainstem, the cerebellum, both PCA territories, the right MCA territory, and in part the right ACA territory via the right PCoA, which explains the overall high ﬂ ow velocity detected in the right V2-VA.

All the above ﬁ ndings, readily assessable by ultra- sound, however, are only indirect signs of the proximal SA pathology. The occlusive process itself is usually not easy to visualize. The main reason for this is the limited access to the vessel, located behind the clavicle. An absent signal should therefore be cautiously interpreted, while stenoses should be evaluated as soon as increased ﬂ ow velocities and turbulent ﬂ ow can be detected. A SSP can only be expected if a relevant SA stenosis is present. In a correlation study of duplex ultrasound-derived SSP grades and the degree of SA stenosis assessed by angiography, an SA stenosis of at least 60% was found to produce abnormal VA Doppler ﬂ ow signals in 90% of cases. Grade 3 SSP was associated with SA occlusion in most of the observed cases (Yip et al 1992).

It is important to notice that not every severe stenoocclusive process in the SA results in a reversed ipsilateral VA ﬂ ow. Normal VA ﬂ ow directions might be found if other collaterals (e.g., the inferior and external thyroid arteries, the internal mammary artery, or intercostal and ascending arteries) suﬃ ciently compensate for the SA pathology (Berguer et al 1980). Also, vessel disorders and variants of the VA as in ipsilateral VA occlusion, VA terminating as posterior inferior cerebellar artery (PICA), or a VA not originating from the SA but directly from the aortic arch may hinder its function as a collateral vessel.

How do other angiologic methods compare with ultrasound in assessing the above dynamic ﬂ ow patterns? DSA has been considered to be the standard procedure in diagnosis of SSP as it permits direct visualization of

<<< < Предыдущая 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 4344 / 5044 45 46 47 48 49 50 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
30.08.202663 Мб0Книга_5771_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5772_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202657 Мб0Книга_5774_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202656 Мб0Книга_5775_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202653 Мб0Книга_5776_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202651 Мб0Книга_5777_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202648 Мб0Книга_5778_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5779_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202678 Мб0Книга_578_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202642 Мб0Книга_5780_Библиотеки_им_академика_М_И_Перельмана.pdf