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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5770_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •1.1 Earliest History
- •1.3 The 1970s
- •2.4.3 Spatial Resolution
- •2.5.1 Reverberation Artifact
- •2.5.2 Comet-Tail Artifact
- •2.5.3 Mirror-Image Artifact
- •2.5.4 Shadowing Artifact
- •2.5.5 Posterior Enhancement Artifact
- •2.6 Doppler
- •2.7 Summary
- •References
- •Suggested Reading
- •1.5 Expanded Applications
- •References
- •2.1 Introduction
- •2.4.2 Attenuation
- •3.1 General Notes
- •3.3.3 The Lateral Neck Compartment
- •References
- •4: Interventional Ultrasonography
- •4.1 Introduction
- •4.2 General Techniques
- •4.3 Indications
- •4.3.1 Punctures
- •Cytologic Examinations (Fine Needle Aspiration)
- •Histologic Examinations (Core Biopsy)
- •4.4 Catheterization
- •4.4.2 Vascular Access/Cannulas
- •4.6 Technical Remarks
- •References
- •5.1.1 Reactive Lymphadenopathy
- •5.1.2 Tuberculous Lymphadenopathy
- •5.1.3 Non-tuberculous Mycobacteria (NTM) Lymphadenopathy
- •5.1.5 Suppurative Lymphadenopathy (Abscesses)
- •5.1.8 Malignant Lymphoma Nodes
- •5.2.1 Central/Anterior Lymphadenopathy
- •Thyroid Cancer
- •5.2.2 Lateral Lymphadenopathy
- •Thyroid Gland Cancer
- •Non-tuberculous Lymphadenopathy
- •Tuberculous Lymphadenopathy
- •5.2.3 Posterior Lymphadenopathy
- •HNSCC Lymph Node Metastases
- •Tuberculous Lymphadenopathy
- •5.3 Cystic/Necrotic Lymphadenopathy
- •5.3.2 Malignant Lymphadenopathies
- •HPV-Positive Metastases
- •EBV-Positive Metastases
- •Thyroid Carcinoma Lymph Node Metastases
- •Lymphoma Nodes
- •References
- •6.1 General Notes
- •6.3.1 Atheroma
- •6.3.2 Lipoma
- •6.3.4 Fistula
- •6.4.1 Branchial Cysts
- •6.4.2 Thyroglossal Cysts
- •6.5.1 Carotid Body Tumor
- •6.5.2 Neurinoma
- •6.5.3 Rare Tumors
- •6.6 Posttraumatic Changes
- •6.6.2 Foreign Bodies
- •References
- •References
- •8.1 Introduction
- •8.2.1 Pre-styloid Compartment
- •8.2.2 Post-styloid Compartment
- •8.3.1 Clinical Evaluation
- •8.3.2 Physical Examination
- •8.3.3 Family History
- •8.4 Diagnostic Imaging
- •8.5 Sonographic Technique
- •8.5.1 Grayscale Images
- •8.5.2 Doppler Images
- •8.5.3 Sonographic Approach
- •8.7 Primary Lesions
- •8.7.1 Schwannoma
- •8.7.3 Paraganglioma
- •8.7.4 Lipoma
- •8.7.6 Branchial Cleft Cyst
- •8.8 Secondary Lesions
- •8.8.1 Salivary Gland Tumors
- •8.8.2 Nodal Metastasis
- •8.8.3 Abscess
- •8.9 Treatment
- •8.9.1 Surgical Approaches
- •8.10 Conclusions
- •References
- •9.1 Introduction
- •9.2 Suprahyoid Space
- •Neoplasms
- •Suprahyoid Cystic Lesions
- •9.2.2 Masticator Space
- •9.3 Infrahyoid Space
- •10.2 Anatomical Remarks
- •10.3 Technical Remarks
- •References
- •10.1 Introduction
- •10.5.1 Carotid Artery Pathology
- •Carotid Intima-Media Thickness (IMT)
- •Carotid Artery Stenosis
- •10.5.2 Carotid Artery Dissection/Aneurysm
- •10.6.2 Dynamic Sonopalpation
- •10.6.3 Transcranial Doppler Sonography
- •References
- •11.1 Introduction
- •11.2.1 Infectious Sialadenitis
- •Bacterial Sialadenitis
- •Viral Sialadenitis
- •11.2.2 Autoimmune Sialadenitis
- •Sjögren’s Syndrome
- •Sarcoidosis
- •IgG4-Associated Sialadenitis
- •11.2.3 Radiation-Induced Sialadenitis
- •11.2.4 Chronic Recurrent Parotitis
- •11.3 Sialadenosis
- •11.4 Duct-Associated Disease
- •11.4.1 Obstructive Sialadenitis
- •11.4.2 Duct Cysts
- •11.5 Neoplasms
- •11.5.1 Benign Tumors
- •Pleomorphic Adenoma
- •Monomorphic Adenoma
- •11.5.2 Malignant Tumors
- •Lymphoma
- •References
- •12.2.1 Size (Small Nodules, Large Nodules, Large Goiter)
- •12.2.2 Echogenicity (Hyperechoic, Hypoechoic, Isoechoic)
- •12.2.4 Margins (Regular, Suspicious, Irregular)
- •12.2.7 Elastography
- •12.3 Thyroiditis
- •12.4 Graves’ Disease
- •12.5.1 American Thyroid Association (ATA) Guidelines
- •References
- •13.4 Ultrasound Technique
- •13.8 Summary
- •References
- •14.1 Introduction
- •14.2 Anatomical Remarks
- •14.3 Technical Remarks
- •14.4.1 Acute Sinusitis
- •14.4.2 Chronic Sinusitis
- •14.4.4 Postoperative Care
- •14.4.5 Paranasal Sinus Tumors
- •14.6.1 Abscesses
- •14.6.2 Benign Lesions
- •14.6.3 Malignant Lesions
- •14.7.1 Technical Remarks
- •14.7.2 Ultrasound Anatomy
- •Graves’ Ophthalmopathy
- •Orbital Tumors
- •Malignant Tumors
- •Fractures
- •References
- •15: Endoscopic Ultrasound
- •15.1 Introduction
- •15.3.4 Larynx
- •15.3.5 Trachea
- •15.3.6 Hypopharynx
- •15.3.7 Proximal Esophagus
- •15.4 Conclusion
- •References
- •16: Contrast-Enhanced Ultrasonography: Clinical Applications
- •16.1 Introduction
- •16.2.1 Safety Considerations
- •16.2.2 Regulatory Status
- •16.3.1 Salivary Gland Tumors
- •Pleomorphic Adenoma
- •Carcinoma Ex Pleomorphic Adenoma
- •Cystadenolymphoma (Warthin’s Tumor)
- •Sjögren’s Syndrome
- •16.3.4 Lymph Nodes
- •Malignant Lymphomas
- •Carcinoma Metastasis
- •16.3.5 Paragangliomas
- •16.3.7 Tumor Response Assessment
- •References
- •17.1 Introduction
- •17.3 3D/4D Ultrasound
- •17.4 Computerized Ultrasound Image Analysis
- •17.5 Molecular Imaging
- •17.6 Targeted Therapy
- •17.7 Elastography
- •References
- •Index

218
H. J. Welkoborsky
Three-dimensional ultrasound imaging of the vessel is
useful to recognize carotid stenosis. Together with ow pattern, this technique might be important for planning an operative procedure in the future [24].
According to the AIUM and SRU (Society of Radiologists
in Ultrasound) consensus recommendations, carotid artery
stenosis can be graded according to the sonographic characteristics listed in Table10.2a, b [7, 25]:
been performed. In these cases, duplex sonography reveals
information about the revascularization and eventual restenosis [26]. Patients who have received a carotid artery stent
or carotid artery angioplasty for carotid stenosis or aneurysm
should undergo careful long-term follow-up and surveillance, which can be ensured by both duplex sonography and
transcranial Doppler (TCD) sonography [27, 28], dynamic
techniques that are noninvasive and cause no radiation exposure. By B-mode and duplex sonography, the position of the
• Minimal carotid artery stenosis (<40%)
• Mild carotid artery stenosis (40–59%) (Fig.10.15)
• Moderate carotid artery stenosis (60–79%) (Fig.10.16)
• Severe carotid artery stenosis (80–99%) (Fig.10.17)
• ICA occlusion (100%)
stent and its patency can be estimated (Fig.10.18). TCD provides information about the cerebral hemodynamic status
[27, 29]. Duplex sonography can be used to estimate restenosis after stent implantation; the risk is about 6% after 2years
[30, 31]. In a long-term follow-up, increasing peak systolic
velocities and ICA/CCA ratios correlate with evolving reste-
B-mode and duplex sonography is also highly useful in
cases in which endarterectomy or insertion of a stent has
Table 10.2a Grade of ICA stenosis according to NASCET [23]
Grade of
stenosis (%) 10 20–40 50 60 70 80 90 Occlusion
Main
criteria
Additional
criteria
B-mode sonography +++ +
Color-coded sonography + +++ + + + + + +++
Systolic peak ow velocity in the maximum of the
stenosis (cm/sec) ca. (=circa)
Systolic poststenotic peak velocity >50 <50 <30
Collateral vessels and precursors (periorbital
arteries/ACA)
Diastolic prestenotic blood ow deceleration (CCA) (+) ++ +++ +++
Poststenotic ow disturbances/turbulences + + ++ +++ (+)
End-diastolic peak velocity in the maximum of the
stenosis (cm/sec)
“Confetti” sign (+) ++ ++
Stenosis index (ICA/CCA)
nosis in the stented carotid artery [32]. In patients following
carotid arterioplasty, carotid duplex ultrasound identies
200 250 300 350–400 100–500
(+) ++ +++ +++
<100 <100 >100 >100
>2 >2 >4 >4
Table 10.2b Grading and sonographic and Doppler characteristics of carotid artery stenosis [1, 7, 25]
Grade Sonographic characteristics Systolic blood ow velocity
Minimal (<40%) Small atherosclerotic plaque and/or thickening of
Mild (40–59%) Larger atherosclerotic plaques Local increase of peak and mean ow velocities
Moderate (60–79%) Atherosclerotic plaques occlude more than 50% of
Severe (80–99%) Only a minor vessel lumen is visible by B-mode
Complete occlusion
(100%)
CCA common carotid artery, ECA external carotid artery, ICA internal carotid artery
the intima/media
the vessel’s lumen
Distortion of normal ow in addition to an
increase of peak and ow velocities
and color Doppler sonography
No lumen can be detected inside the vessel by
either B-mode or color Doppler sonography
<120cm/s
Systolic blood ow velocity >120cm/s
120cm/s through 250cm/s with systolic ow deceleration in the
poststenotic segment of the vessel
Peak ow velocities exceeding 250cm/s (up to 500cm/s!)
Prestenotic and poststenotic blood ow velocity is signicantly
reduced compared with the unaffected contralateral side
Retrograde ow via the ophthalmic artery may occur
Absence of any signal
A low-velocity signal along with predominant reversed signal
component and absence of diastolic ow can be detected at the
presumed origin of the ICA (stump ow)
The blood ow of the CCA is reduced and a retrograde ow in the
ophthalmic artery may occur.
Elevated diastolic ow velocity in the ECA may occur, indicating
collateral supply via the ophthalmic artery

a
b
10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
219
severe recurrent stenosis, but it also can identify carotid
arteries that will appear normal on arteriography [28]. Hence,
TCD sonography and color duplex sonography are useful in
the diagnosis and risk stratication of patients with carotid
artery disease [29]. In conclusion, ultrasonographic techniques are noninvasive examinations with low cost and good
availability for the initial diagnosis and follow-up of many
carotid artery diseases [33].
Fig. 10.15 Mild carotid artery stenosis (40–59%). To p left, bottom left, and longitudinal view of the carotid artery with a plaque narrowing the vessel’s
lumen by about 50%. Top left, bottom right: the prestenotic and poststenotic blood ow velocity is measured by Doppler. Top right, axial plane
Fig. 10.16 Moderate carotid artery stenosis. The systolic blood ow
velocity in the stenosis is about 200 cm/sec (a). The systolic blood ow
velocity in the poststenotic segment of the vessel is about 100 cm/sec
(b). (Courtesy of Dr. Silke Hörnschemeyer-Decker, Dept. of Neurology,
Nordstadt Clinic, Academic Hospital, Hannover, Germany)

220
H. J. Welkoborsky
10.5.2 Carotid Artery Dissection/Aneurysm
Carotid artery dissection can occur in the intracranial or
extracranial part of the vessel, conditions known as two different disease entities. Extracranial dissection is known to
be one of the most frequent causes for a stroke in young
people [34]. The cause of the dissection might be traumatic,
infectious, or iatrogenic. Sonographically, the lumen of the
vessel can be tapered, and sometimes a oating intimal ap
is seen. The false lumen can lead to a narrowing of the true
Fig. 10.17 Severe carotid artery stenosis (80–99%). (a) The plaque
narrowing the lumen of the vessel signicantly in a longitudinal plane.
The Doppler is recorded prestenotically. (b) Atherosclerotic plaque in
longitudinal plane. (c) Duplex of the vessel with the Doppler in the
stenosis reveals a systolic blood ow velocity of more than 600 cm/sec.
a
b
(d) The systolic blood ow velocity in the poststenotic segment of the
vessel is 50 cm/sec. (Fig. 10.17. (c) and (d): Courtesy of Dr. Silke
Hörnschemeyer-Decker, Dept. of Neurology, Nordstadt Clinic,
Academic Hospital, Hannover, Germany)

10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
221
c
Fig. 10.17 (continued)
lumen (Fig. 10.19). Duplex sonography can reveal either
forward, reverse, or bidirectional ow. Doppler sonography
may show complex ow dynamics that are signicantly
dependent on the presence of a thrombus inside the false
lumen, the existence of an entry and exit ap, and the extent
of the dissection [1]. If surgery is indicated and performed,
monitoring is possible during recanalization and in the
d
postoperative period using B-mode, color-coded, and
Doppler sonography [34]. As a differential diagnosis,
carotid artery dissection must be separated from vascular
abnormalities such as carotid webs [35], which are
extremely rare but can cause quite similar sonographic and
duplex sonographic characteristics [35]. Sonography (especially duplex and TCD sonography) is also suitable to pro-

222
Fig. 10.18 Carotid artery following stent implantation in axial (left) and longitudinal section (right). The stented vessel is patent
H. J. Welkoborsky
vide an insight into the patient’s cerebral perfusion status,
such as following carotid artery stenting [27, 29]. In some
cases of vertebral artery dissection, duplex and TCD sonography provides important information regarding that vessel’s wall and the size of the aneurysm [36].
10.5.3 Thrombosis oftheInternal Jugular Vein
(Including Lemierre Syndrome)
Thrombosis of the internal jugular vein occurs mainly as a
result of cancer, central venous or Swan-Ganz catheters, or
injuries, as part of the ovarian hyperstimulation syndrome, or
as part of an autoimmune disease (e.g., Behçet’s disease).
When it occurs as a septic thrombosis owing to a primary
ear, nose, or throat infection, the disease is called Lemierre
syndrome [37–41]. Lemierre syndrome is very rare, with an
incidence reported to be lower than one in a million [42].
Multivariate analysis revealed the following risk factors for
an internal jugular vein thrombosis: older age, female sex,
and ovarian hyperstimulation syndrome [40].
Microvascular head and neck reconstruction with venous
draining of the ap into the internal jugular vein can also
cause thrombosis, even several days postoperatively [43].
B-mode ultrasound and color-coded ultrasound can be
applied as a useful tool to assess the patency of the ap’s vessels and anastomosis.
Lemierre syndrome is typically caused by an infection
with Fusobacterium necrophorum; the portal of entry is
often located in the oropharynx rather than in other pharyngeal structures such as the hypopharynx or the oor of the
mouth [42, 44]. The infection leads rst to a phlebitis, with
thrombosis following.
Thrombosis of the internal jugular vein can have lifethreatening complications, including sepsis, pulmonary
embolism, and post-thrombotic syndrome [40]. The mortality rate was reported to be 90% in the pre-antibiotic era [38].
Therapy for Lemierre syndrome consists of intravenous antibiotics for about 10–14days, followed by oral antibiotics for
up to 6weeks [44]. Anticoagulative agents are also recommended [38] and represent the main therapy in cases of aseptic internal jugular vein thrombosis.
Diagnosis of internal jugular vein thrombosis can be
made rapidly by B-mode and color-coded sonography. The
thrombus appears as a hypoechoic mass inside the vessel’s
lumen, attached to the vessel’s wall. In cases of thrombophlebitis, a signicant thickening of the vessel’s wall can
occur. The vein is often dilated distally to the thrombus; in
cases of complete occlusion, it shows no blood ow proximal to the thrombus [39, 42, 44] (Fig. 10.20; Video 10.6).
Additional investigation of the internal jugular vein on the
opposite side is also recommended, as well as an examination of the proximal parts of the vessel and the subclavian
vein, as some thrombosis can extend proximally into the
subclavian vessels [39]. In these cases, CT angiography
delineates the extension of the thrombosis better than
B-mode sonography and color-coded sonography alone [39].
In cases of incomplete vessel occlusion, color-coded sonog-

ab
10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
Fig. 10.19 Carotid artery
dissection. (Courtesy of Peter
Jecker, MD, PhD; also see
Chap. 6)
223
Fig. 10.20 Septic thrombosis of the internal jugular vein (IJV) as a result of a peritonsillar abscess (Lemierre syndrome). The thrombus displays
as a mass inside the vessel’s lumen. (a) Axial plane. (b) The thrombus inside the vessel in the longitudinal plane
raphy reveals the hypoechoic thrombus, which is surrounded
by some blood ow.
10.6 Inltration ofLarge Neck Vessels by
Malignant Tumors
B-mode sonography, color-coded sonography, and, if
zation during therapy and in the post-therapeutic follow-up.
In patients with bilateral idiopathic internal jugular vein
thrombosis, cancer (especially lung cancer) or malignant
lymphoma must be excluded [40].
possible, the B-ow mode are essential to monitor recanali-
The diagnostic accuracy of ultrasound in the detection of
lymph node metastases is unmistakable in the literature.
One of the most important issues for ultrasound application
in the head and neck is the estimation of suspected vessel
inltration by a tumor in patients with very large metastases

224
H. J. Welkoborsky
Table 10.3 Direct and indirect sonographic signs of vessel
inltration
Direct signs
Direct inltration of the vessel’s wall
Visible tumor parts inside the vessel’s lumen
Lack of shifting between tumor and vessel estimated by dynamic
sonopalpation
Indirect signs
Cranio-caudal contact zone between vessel and tumor of >3cm
Tumor surrounding the vessel by >180°
Fig. 10.21 Indirect sign of vessel inltration by a malignant tumor:
cranio-caudal contact zone of >3cm. In this case, a particular tissue
layer between the vessel and tumor is visible, which makes an inltration unlikely
[45]. Taken together, B-mode sonography, duplex sonogra-
phy, and TCD sonography are more effective than CT scans
in this setting in excluding invasion of the carotid artery by
metastases [46].
10.6.1 Sonographic Criteria forVessel
Inltration
Sonographically, there are direct and indirect signs of vessel inltration by a given tumor, which are listed on
Table10.3. The indirect signs are illustrated by Figs.10.21
and 10.22.
Ultrasound is also suitable for detecting extracapsular
spread of cervical lymph node metastases, with a specicity
of 81.8% and a sensitivity of 78.6% [47]. However, subclinical inltration of the carotid sheath, which is rare, is hard to
recognize by sonography [48]. Color Doppler sonography is
useful to detect the coexistence of sclerotic plaques in the
carotid arteries, which may have consequences for the therapeutic procedure [49].
The suspected vessel inltration can be grouped in ve
stages, as explained in Table 10.4 and illustrated by
Fig.10.23. In stages II and III, dynamic sonopalpation is
required to estimate the likelihood of vessel inltration,
eventually followed by TCD sonography with and without
manual compression of the ipsilateral ICA or balloon
occlusion of the ipsilateral ICA to estimate the contralateral
blood supply to the brain by the contralateral carotid artery
where appropriate [50].
10.6.2 Dynamic Sonopalpation
Dynamic sonopalpation takes advantage of the dynamic
nature of ultrasound examination. It is indicated in all cases
where vessel inltration by a given tumor is suspected (stages
II through IV), before contemplating therapeutic strategy.
The technique of this examination is quite easy: the mass is
visualized on the ultrasound screen in both transverse and
longitudinal sections, and the indirect and direct signs of vessel inltration are determined. The tumor is then palpated
and moved by the examiner’s hand under direct view (Video
10.7). Whether the vessel shifts towards the tumor is documented. A shifting indicates no vessel inltration, and the
tumor can therefore be resected with low risk to the vessel.
On the other hand, lack of shifting indicates vessel inltration. Additional examinations, such as TCD sonography, are
required to determine eventual cross ows or anastomosis,
which would allow the vessel to be resected with a low risk
for a stroke [50].
10.6.3 Transcranial Doppler Sonography
Transcranial Doppler (TCD) sonography is an ultrasound
technique for assessment of blood ow velocities and blood
ow directions and in some cases for detection of emboli in
intracranial arteries [51]. It is performed by insonating the
intracranial vessels through various skull “windows” and
cranial foramina. The aim of this examination is to detect
occlusions and narrowing of major intracranial artery trunks
and to estimate collateral ow through anterior and posterior
communicating arteries [52] without using other tests (such
as the balloon occlusion test) that have a potential risk for
development of symptomatic ischemia [53–55]. For TCD
sonography, a low-frequency ultrasound transducer of 1.5
through 3MHz is used, with which thin bony structures can
be penetrated to insonate the intracranial vessels. It is important to note that this examination is done without visual guidance [1, 56]. The insonation of intracranial vessels is
performed via a temporal, suboccipital, orbital, and submandibular window, through which different intracranial vessels
can be assessed [27] (Table10.5).

10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
Fig. 10.22 Indirect sign of
vessel inltration by a
malignant tumor. (a)
Surrounding of the vessel by
the tumor of more than 180°.
(b) Color Doppler. The vessel
is, although surrounded by the
tumor, patent, and there is a
tiny tissue layer between
tumor and vessel
225
a
Table 10.4 Sonographic stages of vessel inltration by a neck tumor and required actions
Stage Sonographic characteristic Action required
Stage 0 No signs of vessel inltration by the tumor The tumor can be resected with no risk or only low risk of vessel injury
Stage I Sharply demarked tissue layer between the tumor and
the vessel; good shifting of the tumor toward the
vessel estimated by dynamic sonopalpation
Stage II Unsharp tissue layer between tumor and the vessel Dynamic sonopalpation is required to estimate the vessel inltration
Stage III Unsharp tissue layer between tumor and the vessel; no
signicant shifting between the tumor and the vessel
estimated by dynamic sonopalpation
Stage IV Tumor masses inside the vessel’s lumen Vessel inltration is proven
The tumor can be resected with low risk of vessel injury or a stroke
When there is a signicant shifting of the tumor toward the vessel, the
tumor can be resected with low risk for vessel injury
Vessel inltration by the tumor is highly probable
Transcranial Doppler sonography with compression test is required to
estimate a cross ow prior to surgical intervention
Transcranial Doppler sonography with compression test; if this is not
possible, more invasive tests (e.g., balloon occlusion test) are required
prior to surgery to estimate a cross ow and therefore the risk that the
patient will suffer a stroke
b

226
Fig. 10.23 Stages of vessel
inltration by a malignant
tumor. (a) Stage I: sharply
demarcated tissue layer
between tumor and vessel. (b)
Stage IV: tumor masses inside
the vessel’s lumen
H. J. Welkoborsky
a
For identication of the vessels assessed, the distance of
the signal from the probe, ow velocity, ow direction
(toward or away from the probe), waveforms of the Doppler
signal, and pulsatility indices are used. Some authors have
dened normal values for easier identication of particular
vessels and for better interpretation of results [1, 57, 58]
(Table10.6).
b
The indications for TCD sonography examinations com-
prise mainly of neurological diseases [1, 29, 33, 51, 56, 57]:
• Assessment and follow-up of intracranial stenosis and
vessel occlusion
• Assessment of patients with vasospasm in subarachnoid
hemorrhage

10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
227
Table 10.5 “Windows” for transcranial Doppler sonography (TCD)
and vessels that can be assessed [27]
“Window” for TCD Vessels That Can Be Assessed
Temporal approach Internal carotid artery
Orbital approach Ophthalmic artery
Suboccipital approach (via
foramen magnum)
Submandibular approach Distal parts of the extracranial
Table 10.6 Normal distances, blood ow velocities, and ow direc-
tion of some intracranial vessels, assessed by TCD [1, 58]
Distance to
transducer,
Vessel
Middle
cerebral
artery
Anterior
cerebral
artery
Posterior
cerebral
artery
Vertebral
artery
Basilar artery 80– >100 30–50 Away from transducer
Ophthalmic
artery
Internal
carotid artery
TCD transcranial Doppler
mm
40–60 40–80 Toward transducer
60–75 40–60 Away from transducer
60–70 30–50 Bidirectional
50–80 30–50 Away from transducer
30–50 20–30 Toward transducer
60–70 30–50 Away from transducer or
Middle cerebral artery
Anterior cerebral artery
Posterior cerebral artery
Siphon of internal carotid artery
Vertebral arteries
Basilar artery
internal carotid artery
Mean blood
ow
velocity,
cm/s Flow direction
bidirectional, depending
whether temporal or
orbital is measured
tion. TCD sonography is performed when dynamic
sonopalpation reveals a suspicion of vessel wall inltration,
because that vessel probably will need to be sacriced during
operative therapy (Fig. 10.24). The TCD results, together
with a manual compression test or balloon occlusion, are
then strong indicators to estimate the risk of a stroke [50].
The examination begins initially without any manipulation.
In the second step, the ipsilateral carotid artery can be compressed, and it is observed whether there is a cross ow from
the contralateral side into the median cerebral artery. When
there is lack of cross ow, or if the patient develops neurological symptoms, the compression is released. If there is no
cross ow or collateral ow in TCD, a nonfunctional
anastomosis via the communicating arteries is probable [59].
Then the risk for a stroke is very high, and the vessel probably cannot be sacriced. If TCD reveals a cross ow or collateralization, that is a sign of a functional collateral pathway
in the circle of Willis [59], and it may be possible to resect
the vessel with a low risk of stroke [9, 60]. Mean blood ow
velocity reduction of 30% or less during compression or balloon occlusion indicates a low risk for developing neurological symptoms, but mean blood ow velocity reductions of
more than 50% indicate a high risk for developing neurological symptoms [61]. Balloon occlusion has been proven to be
a little more accurate in predicting the occurrence of cerebral
ischemic lesions when the vessel has to be sacriced [62]. In
conclusion, TCD with and without compression offers a noninvasive source of valuable information about perfusion status in patients with large neck tumors inltrating the CCA
and/or ICA.TCD with a carotid compression test is a valid
method for predicting interhemispheric ow and clinically
relevant hemodynamics [54]. The results are comparable to
those obtained by more invasive techniques such as balloon
occlusions [62–64].
• Detection of microemboli during carotid artery or cardiac
surgery
• Assessment of cerebral vasomotor reactivity
• Detection of intracranial aneurysms
• Detection of right-to-left shunts
• Investigation of patients with sickle cell disease to evaluate stroke risk
• Investigation of arteriovenous malformations
• Adjunct in diagnosis of brain death
• Evaluation of positional vertigo or syncope
• Evaluation of collateral pathways for intracranial blood
ow
For head and neck surgeons, it is of great importance to
know whether there is a collateral blood ow and a cross
ow from the collateral carotid artery into the ipsilateral vessel in cases of a tumor with suspected carotid artery inltra-
10.7 Ultrasound Characteristics ofLarge
Neck Vessels Following Surgery or
Radiotherapy
Both surgery and radiation therapy lead to alterations of the
anatomy in the neck. Sonographic orientation can be challenging because of an increase of scar and brous tissue and
the excision of some structures during surgery. The CCA,
which is usually not affected by an operation, is the best anatomic landmark for orientation.
Radiotherapy has a signicant impact on the carotid
artery [65, 66]. In general, radiotherapy leads to an increase
of scar tissue and brosis in the neck and to increases of
intima-media thickness (IMT), plaque size, and plaque
volume in all segments of the carotid artery [67–69]
(Fig. 10.25). The increase in IMT seems dose-related; the
higher the radiation dose, the higher the risk for increased
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