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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5770_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

228
ab
cd
ef
H. J. Welkoborsky
Fig. 10.24 Transcranial Doppler (TCD) sonography to estimate cross
ow in the medial cerebral artery in cases with occlusion of the ipsilateral
internal carotid artery. (a) Stenosis of the common carotid artery on the
right side with blood ow prestenotically (longitudinal plane). (b) Blood
ow in the ipsilateral external carotid artery by duplex and Doppler. (c)
Blood ow in the common carotid artery is prestenotically normal. (d)
Internal carotid artery on the right side is distally occluded, and distal to
the carotid bifurcation, there is a complete obstruction of the vessel. (e)
Duplex sonography reveals normal blood ow in the contralateral (left-
sided) internal carotid artery. Only some at, brotic plaques occur in the
vessel. In this case, blood ow in the medial cerebral artery on the left
side is normal (f), and a moderately good cross ow with collateration of
the median cerebral artery (MCA) on the left side (g) that occurs via the
left anterior communicating artery (or ramus) (ACA) can be detected (h),
which retrogradely lls the right ACA (i) (Courtesy of Dr. Silke
Hörnschemeyer-Decker, Dept. of Neurology, Nordstadt Clinic, Hannover,
Germany). (j) and (k) MRI shows the occluded carotid artery on the right
side in axial view and with vessel reconstruction

jk
10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
229
g
h
i
Fig. 10.24 (continued)

230
Fig. 10.25 Ultrasound of the
neck following radiation
therapy. Note the increase of
scar tissue and brosis. The
internal jugular vein is
missing, as it has been
removed during a neck
dissection. The common
carotid artery is seen with an
increased intima-media
thickness and a calcied
plaque
H. J. Welkoborsky
IMT and plaque formation. Therefore it is important to keep
in mind that after radiation therapy of the neck, patients have
a higher risk of carotid artery disease, especially accelerated
atherosclerosis, so they need intensive follow-up and surveillance. Parallel to changes in the carotid artery wall and
decrease of vessel diameter, hemodynamic changes occur,
with a decrease of blood ow volume following radiotherapy
[70]. If the carotid artery was spared by using intensity-modulated radiotherapy, these pathologic conditions can be signicantly decreased, with both better blood ow volume and
decreased risk of progressive atherosclerosis [71]. Carotid
IMT has been proven to be a strong biomarker for early diagnosis of vascular changes and risk of cerebrovascular events
after radiation therapy of the neck. In these patients, longterm follow-up including B-mode and duplex sonography is
required for early detection and surveillance of vessel
disease.
10.8 Examination ofVessels Prior
toMicrovascular Flap Surgery
Another indication for vessel ultrasound is the identication of the afferent and efferent vessels prior to intended
microvascular tissue transfer. An example is the microvascular forehand ap, which has the radial artery as its feeder
vessel. This is the microvascular ap that is currently most
often used for reconstruction of larger defects in the head
and neck, so it is very common. The examination can be
performed preoperatively and intraoperatively. With this
test, which is called the Allen test, the existence and patency
of the anastomosis between the supercial palmar arterial
arch and the profound palmar arterial arch in the ipsilateral
hand is assessed (Fig.10.26; Video 10.8). The existence of
an anastomosis between the radial and ulnar artery is
required before the ap (which is usually pedicled at the
radial artery) can be harvested. The profound palmar arterial arch is a prolongation of the radial artery and courses
beneath the long exor strings. It is identied on the ultrasound screen, and then the radial artery is compressed
under continuous observation of the blood ow in the palmar arch. The test is positive if there is signicant blood
ow during compression. It is advantageous to perform
pulse oximetry with a sensor at the index nger during the
test, because this provides additional information about the
pulsation, oxygen saturation, and perfusion of the nail bed
during compression of the radial artery. It is very likely that
the blood supply of the second and third nger is sufcient
and the anastomosis is intact when no signicant decrease
of the pulsation curve occurs. The ap can then be
harvested.
Postoperatively, duplex sonography helps to evaluate the
blood supply of an incorporated ap and assess the patency
of the ap’s vessels.

10 Sonography oftheLarge Neck Vessels andofTumors withSuspected Inltration oftheLarge Neck Vessels
Fig. 10.26 (a) Before
harvesting a forehand ap, the
Allen test is performed to
assess the profound palmar
artery arch for collateral
blood supply of the rst three
ngers during compression of
the radial artery. (b) Duplex
sonography reveals a good
blood ow in the profound
palmar arterial arch
a
231
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Sonography ofMajor Salivary Glands
AndreasKnopf
11
Major salivary glands represent a melting pot of inammatory, neoplastic, and dysontogenetic diseases. Diagnostic
approaches are of major clinical impact to achieve both sufcient radicality of epithelial malignancy and a minimum of
functional loss in benign lesions. Whereas B-mode ultrasound demonstrates high sensitivity and specicity in the
identication of sialolithiasis, B-mode ultrasound and colorcoded duplex sonography fail to reliably distinguish inammatory and neoplastic conditions. Recent advances in
elastography increased precision of diagnostic regimens in
inammatory conditions but require great personal expertise.
Modern diagnostic algorithms including elastography and
contrast-enhanced ultrasound result in signicantly higher
precision in the identication of glandular malignancy.
However, complex algorithms are not part of the daily ultrasonographic routine, and detailed anamnesis and clinical
examination remain mandatory in these cases.
11.1 Introduction
Major salivary glands represent a melting pot of inammatory, neoplastic, and dysontogenetic diseases [1–3]. Final
treatment regimens range from wait and scan concepts to
ablative surgery and subsequent facial reconstruction. The
close relation of major salivary glands to vascular and neuronal structures—particularly the facial, hypoglossal, and
lingual nerves—gives rise to the necessity of a reliable
preoperative lesional estimation to manage the balancing
A. Knopf (*)
Department of Otorhinolaryngology–Head and Neck Surgery,
University of Freiburg, Freiburg, Germany
act between sufcient radicality and a minimum of functional loss. High-resolution ultrasound provides detailed
information about the lesional localization, size, shape,
homogeneity, and pattern of vascularity [4]. More recently,
modern ultrasound techniques including strain and shearwave elastography or contrast-enhanced ultrasound
(CEUS) have been applied to increase diagnostic sensitivity and specicity, but these techniques are not part of
today’s routine in major salivary gland ultrasound. MRI
represents an appropriate alternative to head and neck
ultrasound [4–6] and is the diagnostic technique of choice
when complete ultrasonographic visualization fails [5].
CT scans are indicated when a growing tumor is suspicious for osseous destruction. The diagnostic impact of
other imaging techniques (such as glandular scintigraphy
in Sjögren’s syndrome) has decreased in the past decades,
owing to the increased sensitivity and specicity of highresolution B-mode ultrasound [7, 8]. Nevertheless, no
imaging technique is currently able to reliably distinguish
among the variety of salivary gland diseases, so it is vital
to associate salivary gland imaging with the patient’s
detailed history and clinical examination [9, 10].
11.2 Inammatory Diseases
Inammatory diseases of major salivary glands can be
divided into infectious and autoimmune conditions. Other
diseases become clinically apparent as inammation, but
their etiopathogenesis is poorly understood. Traditionally,
the clinical course of salivary gland inammation differentiates between acute and chronic disease, but a substantial proportion of autoimmune diseases that are summarized as
chronic sialadenitis show an acute and self-limiting early
disease stage referring to acute sialadenitis. Therefore, classication in this chapter will reect etiopathogenetic
considerations.
© Springer Nature Switzerland AG 2019
H. J. Welkoborsky, P. Jecker (eds.), Ultrasonography of the Head and Neck, https://doi.org/10.1007/978-3-030-12641-4_11
235

236
A. Knopf
11.2.1 Infectious Sialadenitis
Bacterial Sialadenitis
There are different mechanisms resulting in a bacterial
infection of major salivary glands. Bacteria ascending via
salivary ducts represent one of the most important mechanisms. Dysfunctional saliva drainage and irrigation due to
obstructive sialadenitis, duct ectasia, duct cysts, dehydration, and Sjögren’s syndrome are preconditions in bacterial sialadenitis [11]. Usually, patients present reddened,
enlarged, and painful salivary glands. Pus can be expressed
at the ductal oricium after palpation. However, in parotid
gland sialadenitis, purulent drainage fails if bacterial
infection primarily affects intra-parotideal lymph nodes.
Cutaneous foci frequently result in the affection of the
lymphatic basin of the parotid gland. Hematogenous and
lymphatic spread in salivary glands can be diagnosed in
mycobacteria and mycobacteria other than tuberculosis
(MOTT). Both mycobacteria and MOTT often demonstrate severe resistance to common antibiotics, sometimes
with organ stulation. Abscess formation complicates
bacterial sialadenitis in all pathomechanisms. Bacterial
smear usually identies Staphylococcus aureus and species of the oral ora [12].
B-mode ultrasound visualizes uncomplicated sialadenitis as diffuse and inhomogeneous enlargement of the
glandular tissue [12]. Strand-like hypoechogenicity refers
to congested lymphatic septa (Fig. 11.1). Echo-free
strands referring to congested Wharton’s and Stenson’s
duct can be identied in obstructive sialadenitis. Peripheral
concrements show cortical reex and acoustic shadow
with subsequent proximal duct dilatation (see Sect. 11.4.1)
[13]. Color-coded duplex sonography (CDS) shows glandular hypervascularity (Fig.11.2). Intraglandular abscess
shows irregular borders and marked hypoechogenicity
(Fig.11.3). Inhomogeneity is due to different amounts of
purulent areas. CDS demonstrates peripheral vascularity
and an avascular core (Fig. 11.4). Cold abscesses with
intraglandular stula often occur in mycobacterial/MOTT
sialadenitis (Fig. 11.5). Usually, bacterial sialadenitis is
completed by reactive intra- parotideal and/or cervical
lymphadenopathy.
Fig. 11.2 Color-coded duplex sonography of bacterial sialadenitis
shows marked hypervascularity of the entire left parotid gland, with
hypoechoic lymphatic septa. JA jaw angle
Fig. 11.1 B-mode ultrasound of bacterial sialadenitis shows diffuse
enlargement of the entire left parotid gland with hypoechoic lymphatic
septa. JA jaw angle
Fig. 11.3 B-mode ultrasound of left parotid gland abscesses visualizes
hypoechoic or echo-free lesions with irregular borders. JA jaw angle,
MM masseter muscle

11 Sonography ofMajor Salivary Glands
237
Viral Sialadenitis
Various viruses may infect the major salivary glands. EpsteinBarr virus (EBV), cytomegalovirus (CMV), HIV, and mumps
viruses are the most frequent pathogens [14, 15]. CMV, EBV,
and mumps infections result in acute sialadenitis, but HIVinduced sialadenitis usually presents a chronic clinical course
[14]. In contrast to bacterial sialadenitis, viral infection usually demonstrates oligo-sialadenitis. B-mode ultrasound and
CDS can visualize diffuse and inhomogeneous enlargement of
the glandular tissue with strand-like hypoechogenicity with
marked hypervascularity, comparable to bacterial sialadenitis
(Fig.11.6). However, CMV and EBV demonstrate a predilec-
tion for cervical lymph nodes and therefore parotid gland
infection referring intra- parotideal lymph nodes (Fig. 11.7).
Interestingly, the sonographic appearance of HIV infection
differs signicantly from the other viral infections, demonstrating echo-free areas referring to lymphoepithelial lesions
(Fig. 11.8). CDS and CEUS validate cystic areas without
macro- or micro- perfusion (Fig.11.9). Cystic areas were visualized soft in strain elastography (Fig.11.10). Sonography in
HIV-induced sialadenitis cannot be distinguished from
Sjögren’s syndrome or mucosa-associated lymphoid tissue
(MALT) lymphoma; differential diagnosis is mandatory in
these cases [11, 16–18].
Fig. 11.4 Color-coded duplex sonography (CDS) of left parotid gland
abscesses demonstrates peripheral hypervascularity of avascular echofree areas. JA jaw angle, MM masseter muscle
Fig. 11.5 B-mode sonography of parotid gland tuberculosis shows
echo-free stulae in central glandular parts. CM collum
mandibulae
Fig. 11.6 Oligo-sialadenitis of the parotid gland (PG) and subman-
dibular gland (SMG) in mumps infection. B-mode ultrasound shows
hypoechoic lymphatic septa of the parotid gland and hypoechogenicity
of the submandibular gland
Fig. 11.7 Color-coded duplex sonography of intra-parotideal lymph
node EBV infection. Hypoechoic lymph nodes show hilus hypervascularity. JA jaw angle

238
A. Knopf
11.2.2 Autoimmune Sialadenitis
Sjögren’s Syndrome
Sjögren’s syndrome represents the most important rheumatic
disorder affecting the head and neck, with a prevalence of
1–2% in the adult population, a female predominance of
approximately 8:1, and a mean age of onset usually in the
fourth to fth decade of life [11, 19, 20]. Sjögren’s syndrome
can be present without another underlying inammatory
condition (primary Sjögren’s syndrome), or it may be coupled with an underlying inammatory disease (secondary
Sjögren’s syndrome). Autoantibodies induce chronic epithelialitis, particularly of serous salivary glands. Therefore, the
parotid and lacrimal glands are predominantly affected, but
sialadenitis also includes submandibular, sublingual, and
minor salivary glands [11, 17]. Chronic glandular inammation results in an insidious destruction of salivary gland tissue and progressive sicca symptoms. Acute and self-limiting
enlargements of major salivary glands, particularly of the
parotid gland, represent typical symptoms of early disease
stages, but they are dramatically underdiagnosed [11, 17].
Bilateral, hypoechoic lesions of the submandibular and
Fig. 11.8 B-mode ultrasound of lymphoepithelial lesions in HIV
infection demonstrates multiple intra-parotideal echo-free areas. JA jaw
angle
Fig. 11.9 Color-coded duplex sonography of lymphoepithelial lesions
in HIV shows peripheral hypervascularity and avascular echo-free
areas. JA jaw angle
Fig. 11.10 Strain elastography of lymphoepithelial lesions in HIV infection. Echo-free areas are visualized soft (blue) in contrast to hardened
parotid gland tissue (red). Red areas in the lymphoepithelial lesion refer to compression phenomenon to incompressible liquids
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