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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3643_Библиотеки_им_академика_М_И_Перельмана.pdf
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The two subclavian arteries have different origins. The
right SCA is readily approachable at cervical level, while the
origin of the left is not. Indirect signs of SCA stenosis are
available: post-stenotic fl ow evidenced on the distal SCA
and axillary or better on the brachial artery. A different blood
pressure in the two arms raises the suspicion of SCA stenosis
or aortic dissection, and sometimes, it is diffi cult to tell the
difference between the two conditions without performing
the CT or TEE. Stenosis of the origin of the left SCA can be
also accompanied by similar lesions at the origin of the BCT
and of the aortic arch, even if the origin of the right SCA and
of the right CCA is not (severely) diseased. Patterns of fl ow
more diffi cult to interpret may appear with an atherosclerotic
ARSA and Kommerell diverticulum.
Stenosis of the SCA proximal to the origin of the VA may
be accompanied by the subclavian steal syndrome . This syn-
drome does not appear in all cases, as its presence depends
on the caliber and length of the VA of the same side: the
syndrome will not develop in case of hypoplastic VA or in
case with a left VA with aortic origin. Moreover, not all
patients with steal syndrome are symptomatic (and asymptomatic cases should not be operated). In other circumstances, the proximal segments of the VA are also occluded
(V0 and V1 and sometimes even the V2), while the subclavian steal is apparent, through highly developed collaterals
between the V3, ECA, and SCA on the same side (see Chap.
7 for details). Consequently, the ultrasound diagnosis of
SCA stenosis and the presence of steal syndrome is not
always at hand and not always achievable in its totality. The
steal syndrome may fl uctuate with the cardiac cycle (positive
systolic complexes alternating with negative diastolic complexes, in the SCA) and may diminish while performing the
cuff test (the cuff of the sphygmomanometer is infl ated above
the systolic blood pressure). Retrograde fl ows in the VA are
characteristic and may be elicited over the V2 segment of the
VA and more diffi cult at the level of the V3. With TCD the
V4 segment and the BA may be approached, certifying the
steal syndrome (basilar steal syndrome). In experienced
hands even a laminar fl ow in the BA can be elicited with different directions of fl ow in the right and left sides of the
BA. At TCD, the cerebellar arteries originating on the side
with subclavian steal depict a post-stenotic pattern of fl ow.
The postoperative/post-endovascular treatment is rou-
tinely assessed by ultrasound. Ultrasound in the follow-up of
patients represents a valuable tool (Figs. 5.21 , 5.22 , 5.23 ,
5.24 , 5.25 , 5.26 , and 5.27 ). We usually recommend the fi rst
control at approximately 1 month after patient’s discharge
and afterward, on a biannual basis. The numerous types of
arterial reconstruction can be readily checked and measured,
including the CAS. Complications, technical failures, accelerated atherosclerotic process, and the development of
plaques in untreated arterial segments are all readily diagnosed by ultrasound. Another important parameter in the
evaluation of the results of the therapy is represented by the
measurement of the IMT. We recommend guiding statin
therapy by taking into account not solely the lipid profi le but
also considering the IMT.
The spontaneous contrast in the IJV (see Fig.
5.28 for
details) may appear as an accidental fi nding or during the
postoperative checkup. It is still diffi cult to assign a precise
cause to the phenomenon or to indicate a particular treatment. Patients must be evaluated for a possible hypercoagulable state. The spontaneous IJV contrast may also appear in
cases with a notable asymmetry of the two IJV.
Conclusive Remarks In contemporary medicine, it is
highly advisable that clinicians train in and perform one
imaging technique. Ultrasound appears more at hand as
compared with angiography or CT (and does not require a
radiological competence, including a longer training); ultrasound appears even more clinically related as compared with
the alternative diagnostic modalities. Ultrasound can be performed on ambulatory basis too. However, as stated before,
the clinician should ideally be a neurologist or cardiologist
well trained and a connoisseur of the anatomy and clinical
manifestations of the cerebrovascular diseases. Conversely,
specialists dedicated to diagnostic imaging must be endowed
with all the particulars regarding the clinical status of the
patient; otherwise, the fi nal image will be a standard one
with least practical signifi cance. As a consequence, a pertinent and continuous dialogue must be established between
all the specialists who diagnose and treat cerebrovascular
diseases.
In spite of the advantages offered by the versatility of the
technique, the lower costs, the reduced space for lodging the
ultrasound equipment and for patient examination, the echographical approach, and the fi nal diagnosis are dependent, in
a very high degree, on the operator. Not least, the operator
should be looked upon as the member of a complex team of
specialists approaching the patient with cerebrovascular diseases from different angles but focusing on a common target
which is the best therapy with the best outcome.
5 Diagnostic Approach to Cerebrovascular Disease: Ultrasound
114
Fig. 5.1 Normal fl ow pattern – carotid artery. Laminar fl ow at the level
of the carotid and ophthalmic arterial axis. Note the “ultrasonic window” at the level of the ICA (base of the spectral frequencies), refl ect-
ing a normal fl ow pattern. CCA common carotid artery, ICA internal
carotid artery, ECA external carotid artery, OA ophthalmic artery, L left,
R right
Image Gallery
A. Nistorescu and H. Muresian
115
Fig. 5.3 Superior thyroid artery.
Passage of the ultrasonic wave
from the superior thyroid artery
(STA) to the carotid. In many
patients the laterocervical bruit
originates in the STA. The STA
serves as a good marker for the
carotid bifurcation
Fig. 5.2 Normal fl ow pattern – subclavian and vertebral arteries. The normal fl ow pattern in the subclavian artery ( SCA ) and vertebral artery ( VA )
5 Diagnostic Approach to Cerebrovascular Disease: Ultrasound
116
Fig. 5.4 V3 segment of the VA. The atlas loop appears with both a positive and negative signal pattern
Fig. 5.5 TCD – ophthalmic window. Imaging of the intracerebral segments of the ICA. The intracavernous segment (depth 65 mm) appears posi-
tive while the supraclinoid segment, negative. The positive OA and the venous fl ow in the cavernous sinus are discernable at the same depth
A. Nistorescu and H. Muresian
117
Fig. 5.6 TCD – temporal window. The A1 segment of the ACA appears
at a depth of 70 mm ( upper left panel ) with a negative signal.
Compression of the ipsilateral carotid ( upper right panel ) is followed
by the disappearance of signal, refl ecting a nonfunctional PCommA.
The signal over the M1 segment of the left MCA ( lower left panel )
disappears with ipsilateral carotid compression, while the signal over
the P1 segment of the PCA increases in amplitude, refl ecting a patent
and effi cient PCommA on the same side ( lower right panel )
5 Diagnostic Approach to Cerebrovascular Disease: Ultrasound
118
Fig. 5.8 TCD – the basilar artery. The BA appears with a negative
signal at a depth of 75–120 mm ( upper left panel ). The positive signal
is from one of the superior cerebellar arteries ( upper right panel ). The
PCommA appears with a positive signal at a depth of 100–120 mm. The
bifi d BA represents a normal variation of this artery ( lower panel )
Fig. 5.7 TCD – occipital window. The V4 segment of the V4 can be
imaged through the foramen magnum at a depth of 50–65 mm (negative
signal, left panel ). Increases in velocity in V4 after ipsilateral carotid
compression refl ect a patent and functional PCommA. The PICA can be
individualized after orienting the probe slightly lateral, at a depth of
65 mm
A. Nistorescu and H. Muresian
119
Fig. 5.9 Transcranial color-coded sonography (TCCS) – orbital win-
dow. The OA ( left panel ) can be imaged with a transocular approach
(orbital window). Using the same approach, the carotid siphon is identi-
fi ed ( right panel ), with a positive signal (the intracavernous segment of
the ICA) and with a negative one (the supraclinoid segment)
Fig. 5.10 TCCS – temporal window (1). The ACA appears in blue color and depicts a negative velocity signal ( left panel ), while the MCA appears
in red color and with a positive signal ( right panel )
Fig. 5.11 TCCS – temporal window (2). The terminal part of the ICA appears with positive signal ( left panel ) and ACA at its origin (with a nega-
tive signal). Through the same window, the P1 segment of the PCA appears with a positive signal ( right )
5 Diagnostic Approach to Cerebrovascular Disease: Ultrasound
120
Fig. 5.12 TCCS – occipital window (1). The VA appears in blue color and negative signal ( left panel ); deeper, the PICA appears with a positive
signal ( right )
Fig. 5.13 TCCS – occipital window (2). The BA is visible at depths between 75 and 120 mm ( negative and blue color ). The SCA is visible at
depths between 80 and 100 mm ( positive – right panel )
Fig. 5.14 TCCS – occipital window (3). The P2 segment of the PCA is visible at depths between 100 and 120 mm ( red color and positive )
A. Nistorescu and H. Muresian
121
Fig. 5.15 Stenosis of the carotid artery (1). ECD with spectral analysis: high-grade stenosis (75–90 %) of the ICA at origin ( left panel ) and imag-
ing of the stenotic area ( right panel )
Fig. 5.16 Stenosis of the carotid artery (2). Higher-grade carotid stenosis (>90 %) with fl ow inversion in the OA ( upper panels ). Aspect of the
plaque and fl ow, in the same patient ( lower panels )
5 Diagnostic Approach to Cerebrovascular Disease: Ultrasound
122
Fig. 5.17 Stenosis of the carotid artery (3). Color-coded image of the
ICA at origin, transversal section ( upper left panel ). The narrow resid-
ual lumen appears (at 3 o’clock) in red-blue color (refl ecting a highly
turbulent fl ow). A high-degree stenosis produced by a homogenous,
hypoechogenic, and voluminous plaque ( right upper panel ). Milder ste-
nosis (grades III–IV) produced by an irregular, nonhomogenous, and
predominantly hypoechogenic plaque (turbulences at the surface of the
plaque; lower panels )
A. Nistorescu and H. Muresian