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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5790_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Acknowledgements
- •Contents
- •1: Theory and Basics
- •1.1.2.3 Reflection
- •1.1.2.4 Absorption
- •1.1.2.5 Deflection
- •1.1.2.6 Focus
- •1.1.2.7 Resolution
- •1.2 Practical Application in US Device
- •1.2.1 Emission, Transmission, Reception and Amplification
- •1.2.1.1 Emission
- •1.2.1.2 Transmission
- •1.2.1.3 Reception
- •1.2.1.4 Amplification
- •1.2.2 Signal Processing
- •1.2.2.1 Preprocessing
- •1.2.2.2 Post-processing
- •1.2.2.3 Time Gain Compensation (TGC)
- •1.2.2.4 Sound Energy = Output
- •1.2.2.5 Gain
- •1.2.2.6 Frame Rate/Persistence
- •1.2.3 Components of US Device
- •1.2.3.1 Transducers
- •Sector Transducers
- •Linear Array Transducers
- •Curved Linear Array
- •Other Transducers
- •1.2.3.2 Other Parts of US Device
- •1.3 US Methods
- •1.3.1 A (Amplitude)-Mode
- •1.3.2 (T)M-Mode (Time-Motion-Mode)
- •1.3.3 B (Brightness)-Mode
- •1.3.4 Doppler Sonography
- •1.4 Artefacts
- •1.4.1 General Remarks
- •1.1 Ultrasound (US) Physics
- •1.1.1 US Waves
- •1.1.2 Propagation and Modulation of US
- •1.1.2.1 Acoustic Impedance
- •1.1.2.2 Impedance Change
- •1.4.2 Common Artefacts
- •1.4.2.1 Side Loop Artefact
- •1.4.2.2 Bowing Artefact
- •1.4.2.3 Noise
- •1.4.2.4 Marginal Shadowing
- •1.4.2.5 Posterior Enhancement – Increased Through Transmission
- •1.4.2.6 Reverberation Artefact
- •1.4.2.7 Increment or Slice Thickness/Beam Width Artefact
- •1.4.2.8 Mirror Image Artefact
- •1.4.2.9 Shadowing
- •1.4.2.10 Refraction Artefact
- •1.4.2.11 Anisotropy
- •1.5 Biologic Effects
- •1.5.1 General Remarks
- •1.5.2 Thermal Effects
- •1.5.2.1 Tissue Heating
- •1.5.2.2 Biological Effects, Tissue Heating
- •1.5.3 Mechanical Effects and Resonance
- •1.5.3.1 Cavitation
- •Acoustic Cavitation
- •Negative Peak Pressure
- •1.5.4 Potential Risks of Diagnostic US
- •1.5.4.1 Specific Risks
- •1.5.4.2 Guidelines and Recommendations
- •1.5.5.1 Mechanical Index (MI)
- •1.5.5.2 Thermal Index (TI)
- •1.5.5.3 Display of Actual Indices
- •1.6 How to Perform Paediatric US
- •1.6.1 Requisites
- •1.6.1.1 Indications
- •1.6.1.2 Environmental Requisites
- •1.6.1.3 Specific Needs in Children
- •1.6.1.4 Specific Needs in Infants and Newborns
- •1.6.2 Positioning
- •1.6.3 Device Handling
- •1.6.4 Transducer Selection
- •1.6.4.1 General Remarks
- •1.6.4.2 Neurosonography
- •1.6.4.3 Small Part US
- •1.6.4.4 Chest US
- •1.6.4.5 Abdominal US
- •1.6.5 Course of Investigation and Measurements
- •1.6.5.1 General Remarks
- •1.6.5.2 Transducer Handling
- •1.6.5.3 Measurements
- •1.7 Documentation and Interpretation
- •1.7.1 Image Documentation
- •1.7.2 Report
- •1.7.2.1 How to Issue a Report
- •1.7.2.2 Diagnosis
- •1.7.2.3 Predefined Reports
- •1.7.2.4 Nomenclature
- •1.8 Doppler Sonography
- •1.8.1 The Doppler Phenomenon
- •1.8.2.1 Continuous Wave Doppler (CW)
- •1.8.2.2 Pulsed Wave Doppler (PW)
- •1.8.2.3 Duplex-Doppler Sonography
- •1.8.2.5 Amplitude-Coded Colour Doppler Sonography (aCDS)
- •1.8.2.6 Other Flow-Sensitive US Techniques
- •1.8.2.7 Important Parameters and Measurements (Fig. 1.16)
- •1.8.3 Artefacts in (Colour) Doppler Sonography
- •1.8.3.1 Aliasing
- •1.8.3.2 Spectral Broadening
- •1.8.3.3 Sample Volume Artefact
- •1.8.3.4 Filtering Artefacts
- •1.8.3.5 Scaling Problems
- •1.8.3.6 Gain-Induced Errors
- •1.8.3.7 Angle Correction
- •1.8.3.8 Motion Artefact
- •1.8.3.9 Twinkling Artefact
- •1.8.3.10 Others
- •1.8.4 How to Perform (Colour) Doppler Investigations
- •1.8.5 Limitations
- •1.8.6 Interpretation
- •1.9 Modern and Future US Methods and Techniques
- •1.9.1 High-Resolution US (HR-US)
- •1.9.2 Image Compounding
- •1.9.3 Harmonic Imaging (HI)
- •1.9.4 Extended Field of View US
- •1.9.5 US Texture Analysis
- •1.9.6 Sonoelastography
- •1.9.7.1 Basics
- •1.9.7.2 Applications
- •Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •Other Intracavitary Use of ce-US: Sono-Genitography, Sonographic Pyelography, Etc.
- •Intravenous ce-US (CEUS)
- •Future ce-US Potential
- •1.9.8 Three- and Four-Dimensional US (3D-/4DUS)
- •1.9.8.1 Physics and Techniques
- •1.9.8.2 Typical Paediatric 3DUS Applications
- •Neonatal Neurosonography
- •3DUS of the Kidney
- •Urinary Bladder 3DUS
- •3DUS of the Paediatric (Female) Genitalia
- •Musculoskeletal 3DUS Applications
- •Small Part 3DUS Applications
- •Other Potential 3D-/4DUS Applications
- •1.9.8.3 Benefits of 3D-/4DUS
- •1.9.8.4 Restrictions of 3D-/4DUS
- •2: Ultrasound-Guided Interventions
- •2.1 General Aspects
- •2.1.1 Requisites
- •2.1.1.1 Other Important Needs
- •2.1.2 Precautions and Preparations
- •2.2 US-Guided Filling of Structures for Diagnostic or Therapeutic Purpose
- •2.2.2 Diagnostic Sonographic Enema
- •2.2.3 Therapeutic Sonographic Enema
- •2.2.4 US Genitography
- •2.2.5 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •2.2.6 Other Intracavitary Contrast Applications
- •2.2.7 Intravenous ce-US
- •2.3 Biopsies and Punctures
- •2.4 Drainage
- •2.5 Vascular Access
- •2.6 Lumbar Puncture
- •2.7 Foreign Body Removal
- •3: Neurosonography in Neonates, Infants and Children
- •3.1 Requisites
- •3.1.1 Equipment and Transducer Needs
- •3.1.2 Indications for Brain US
- •3.1.3 How to Investigate
- •3.2 Normal Findings
- •3.2.1 Transfontanellar Access
- •3.2.2 Alternate Access Findings
- •3.2.3 Colour Doppler Sonography (CDS)
- •3.2.4 Normal Variances in Preterm Babies
- •3.2.4.1 Periventricular Echogenicities
- •3.2.4.2 Ventricular Asymmetry
- •3.2.4.3 Ventriculomegaly
- •3.2.4.4 Cisterna Magna
- •3.2.4.5 Vascular Variations
- •3.3 Pathologic Findings
- •3.3.1 Neural Tube Defects
- •3.3.1.1 Anencephaly
- •3.3.1.2 Meningomyelocele and Encephalocele
- •3.3.1.3 Arnold Chiari Malformation
- •3.3.1.4 Dandy-Walker Malformations
- •3.3.1.5 Corpus Callosum Malformations
- •3.3.1.6 Lipoma
- •3.3.2 Migration and Gyration Alterations and Disturbances
- •3.3.2.2 Megalencephaly
- •3.3.2.3 Schizencephaly
- •3.3.2.4 Holoprosencephaly
- •3.3.2.5 Hydranencephaly
- •3.3.3 Phakomatoses
- •3.3.4 Cerebral Cysts
- •3.3.5 Ischemic Encephalopathy
- •3.3.5.1 Preterm Infant
- •3.3.5.2 Global or Diffuse Brain Oedema
- •3.3.5.3 Focal Hypoxemia and Ischemia
- •3.3.5.4 (C)DS in Brain Hypoxia
- •3.3.6 Inflammation
- •3.3.6.1 Prenatal Intrauterine Infections and Residuals
- •3.3.6.2 Postnatal Inflammation
- •3.3.7 Dilatation of CSF Spaces: Hydrocephalus
- •3.3.8 Cerebral Haemorrhage
- •3.3.8.2 Haemorrhage in Term Infants
- •3.3.8.3 Role of CDS in Neonatal Haemorrhage
- •3.3.8.4 Haemorrhage in Infants and Older Children
- •3.3.9 Tumours and Space-Occupying Lesions
- •3.3.9.1 Vascular Malformations
- •3.3.10 Cerebral Calcifications
- •3.4 Ultrasound of the Skull
- •3.4.1 Introduction
- •3.4.2 Haematoma
- •3.4.3 Space-Occupying Lesions and Tumours
- •3.4.4 Skull Fracture
- •3.5 Additional Imaging
- •3.5.1 Plain Film
- •3.5.2 CT
- •3.5.3 MRI
- •3.5.4 Catheter Angiography
- •3.5.5 Additional Supporting Procedures
- •3.6 Ultrasound of the Eye and the Orbit
- •3.6.1 Introduction
- •3.6.2 Normal Findings
- •3.6.3 Sonographically Depictable Pathology
- •3.7 Ultrasound of the Spinal Canal
- •3.7.1 Requisites
- •3.7.2 Transducers and Technique
- •3.7.3 Indications
- •3.7.4 Normal Findings
- •3.7.5 Pathologic Findings of the Spinal Cord
- •3.7.5.1 Dysraphism
- •3.7.5.2 Other Associated Pathology
- •3.7.5.3 Other “Occult” Dysraphisms
- •3.7.6 Trauma
- •3.7.7 Tumours
- •3.7.8 Other Spinal and Vertebral Pathology
- •3.7.9 Additional Imaging
- •3.7.10 Value of US
- •4: Ultrasound of the Neck
- •4.1 Indications, Requisites and Techniques
- •4.1.1 Transducers
- •4.1.2 Positioning and Handling
- •4.1.3 Typical Examinations
- •4.1.3.1 Cervical Lymph Nodes
- •4.1.3.2 Glands
- •4.1.3.3 Cervical Arteries
- •4.1.3.4 Cervical Veins
- •4.1.3.5 Intervention
- •4.2 Normal Findings
- •4.2.1 Lymph Nodes
- •4.2.2 Cervical Glands
- •4.2.2.1 Thyroid Gland
- •4.2.2.2 Parotid, Submandibular and Sublingual Glands
- •4.2.3 Other Cervical Soft Tissues
- •4.2.3.1 Muscles
- •4.2.3.2 Tonsils
- •4.2.3.3 Tongue
- •4.2.3.4 Para- and Retropharyngeal Spaces
- •4.2.3.5 Larynx
- •4.2.4 Cervical Vessels
- •4.3 Pathologic Findings
- •4.3.1 Lymph Nodes
- •4.3.2 Pathology of Cervical Soft Tissue
- •4.3.2.1 Malformations
- •Cervical Cyst
- •Dermoid Cyst
- •Duplication Cysts
- •Thymic Cyst
- •Cervical Ectopic Thymus
- •4.3.2.2 Tumours
- •Haemangioma
- •Lymphatic Malformation
- •Other Mesenchymal Tumours
- •Neuroblastoma, (Ganglio-)Neuroma, Neurofibroma and Other Nerve (Sheath) Tumours
- •Teratoma
- •Other Malignant Tumours
- •Role of US
- •4.3.2.3 Abscess Formations
- •4.3.2.4 Traumatic Changes
- •Haematoma (Including Sternocleidomastoid Muscle “Haematoma”)
- •4.3.3 Thyroid Gland
- •4.3.3.1 Cystic Changes
- •4.3.3.2 Malformations
- •4.3.3.3 Inflammation
- •4.3.3.4 Other Conditions
- •Hypothyroidism/Struma Diffusa/Colloides (Fig. 4.17)
- •Nodular Goitre
- •Amyloid Goitre
- •Adenoma/Carcinoma
- •4.3.4.1 Inflammation
- •4.3.4.2 Cysts
- •4.3.4.3 Calcifications/Sialolithiasis
- •4.3.4.4 Tumours
- •4.3.5 Cervical Vessels
- •4.3.5.1 Arteriosclerosis
- •4.3.5.2 Dissection
- •4.3.5.3 Stenosis
- •4.3.5.4 Other Vascular Anomalies
- •4.3.5.5 Thrombosis and Occlusion
- •5: Basics of Paediatric Echocardiography
- •5.1 Introduction
- •5.2 Equipment Needs and Specific Considerations
- •5.2.1 Transducers
- •5.2.2 Standard US Techniques
- •5.2.3 Patient Position
- •5.2.4 Sedation
- •5.3 Standard Planes and Standardised Course of Examination
- •5.4 Normal 2D Echocardiogram Findings
- •5.4.1 Parasternal Views
- •5.4.1.1 Parasternal Long Axis View (Fig. 5.2)
- •5.4.1.2 Parasternal Short Axis Views (Figs. 5.3 and 5.4)
- •5.4.2 Apical Views
- •5.4.3 Subcostal Views
- •5.4.3.1 Sagittal Subcostal View
- •5.4.3.2 Subcostal Four-Chamber View (Fig. 5.6)
- •5.4.4 Suprasternal View (Fig. 5.7)
- •5.5 Other Techniques
- •5.5.1 M (Motion)-Mode Echocardiography
- •5.5.2 Doppler Sonography
- •5.5.2.1 CDS with 2DUS
- •5.5.2.2 PW- and CW-Doppler
- •5.5.2.3 Calculation of Pressure ( P) Gradients ( P 1 Minus P 2)
- •5.5.3 Other Calculations and Functional Parameters
- •5.6 Special Echocardiographic Techniques
- •5.6.1 Transoesophageal Echocardiography (TEE)
- •5.6.2 Three-Dimensional (3D) Echocardiography
- •5.6.3 Tissue Doppler Imaging (TDI)
- •5.6.4 Contrast-Enhanced US
- •5.7 Normal Values
- •5.8 Pathologic Findings
- •5.8.1 Congenital Heart Defects with Left-to-Right Shunt
- •5.8.1.1 Atrial Septal Defect (ASD)
- •5.8.1.2 Atrioventricular Septal Defects (AVSD)
- •5.8.1.3 Ventricular Septal Defects (VSD)
- •5.8.1.4 Patent Ductus Arteriosus of Botalli (PDA)
- •5.8.1.5 Persistent Truncus Arteriosus (Truncus Arteriosus Communis)
- •5.8.2 Obstructions of Left Ventricular Outflow
- •5.8.2.1 Aortic Valve Stenosis (AS)
- •5.8.2.2 Subaortic Stenosis (Sub AS)
- •5.8.2.3 Supravalvular Aortic Stenosis
- •5.8.2.4 Aortic Coarctation (CoA)
- •5.8.2.5 Interrupted Aortic Arch
- •5.8.3 Obstructions of the Right Ventricular Outflow
- •5.8.3.1 Isolated Pulmonary Valve Stenosis (PS)
- •5.8.3.2 Subvalvular Pulmonary Stenosis
- •5.8.3.3 Supravalvular Pulmonary Stenosis
- •5.8.4 Miscellaneous Congenital Heart Defects
- •5.8.4.1 Transposition of Great Arteries (TGA)
- •5.8.4.2 Total Anomalous Pulmonary Venous Return (TAPVR)
- •5.8.4.3 Univentricular Heart (UVH)
- •5.8.4.4 Double Outlet Right Ventricle (DORV)
- •5.8.4.5 Ebstein Anomaly
- •5.8.4.6 Cor Triatriatum
- •5.9 Acquired Paediatric Heart Diseases
- •5.9.1 Cardiomyopathies (CMP)
- •5.9.1.1 Hypertrophic CMP
- •5.9.1.2 Hypertrophic Obstructive CMP (HOCMP)
- •5.9.1.3 Dilated (Congestive) CMP
- •5.9.1.4 Restrictive CMP
- •5.9.2 Acute Myocarditis
- •5.9.3 Acute (Infective) Endocarditis
- •5.9.4 Pericarditis/Pericardial Effusion
- •5.9.5 Kawasaki Disease
- •5.9.6 Intracardiac Thrombi
- •5.9.7 Cardiac Tumours
- •5.10 Complementing Investigations
- •5.10.1 Cardiac Catherisation and Angiography
- •5.10.2 Cardiac MRI and CT
- •5.11 When to Do What
- •5.11.1 Imaging in Typical Clinical Scenarios
- •5.11.1.1 Typical Orientating Examination
- •5.11.1.2 Typical Clinical Queries
- •5.11.2 Trauma and Emergency
- •6: Ultrasound of the Chest
- •6.1 Requisites
- •6.1.1 Transducers
- •6.1.2 Positioning
- •6.1.3 Indications
- •6.1.4 How to Perform Chest US
- •6.2 Normal Findings
- •6.2.1 Chest Wall
- •6.2.2 Breast
- •6.2.3 Pleural Space
- •6.2.4 Diaphragm
- •6.2.5 Lung
- •6.2.6 Mediastinum
- •6.2.6.1 Anterior Mediastinum/Thymus
- •6.2.6.2 Middle Mediastinum
- •6.2.6.3 Posterior Mediastinum
- •6.2.7 CDS
- •6.3 Pathology of Chest Wall
- •6.3.1 Aplasia, Variations of Ribs
- •6.3.2 Congenital Malformations
- •6.3.3 Traumatic Changes
- •6.3.4 Chest Wall Tumours
- •6.3.4.1 Lymphangioma (veno-lymphatic vascular malformation)
- •6.3.4.2 Lipoma
- •6.3.4.3 Fibroma/Neurofibroma
- •6.3.4.4 Other Tumours
- •6.3.5 Breast
- •6.3.6 Role of US and Additional Imaging
- •6.4 Pathology of Pleural Space
- •6.4.1 Pleural Effusion
- •6.4.2 Empyema
- •6.4.3 Other Pleural Pathology
- •6.4.4 Role of Imaging
- •6.5 Pathology of Diaphragm
- •6.5.1 Diaphragmatic Hernia
- •6.5.2 Diaphragmatic Motion Disturbance
- •6.5.3 Role and Potential of Imaging
- •6.6 Lung Pathology
- •6.6.1 Pneumonia
- •6.6.2 Lung Abscess
- •6.6.3 Atelectasis
- •6.6.5 Sequestration
- •6.6.6 Congenital Cystic Adenomatoid Malformation (CCAM)
- •6.6.7 Cysts
- •6.6.8 Infarction
- •6.6.9 Tumours and Space-Occupying Lesions
- •6.7 Other Miscellaneous and Rare Applications
- •Many More Partially Rare Applications Reported: Most Relevant Ones
- •6.7.1 US for Interstitial Lung Disease
- •6.7.2 US for Pneumothorax
- •6.8 Additional Imaging
- •7: Liver and Bile System
- •7.1 Requisites and Investigation
- •7.1.1 Preparation
- •7.1.2 Positioning
- •7.1.3 Transducers
- •7.1.4 Course of Investigation
- •7.1.5 Standard Planes
- •7.2 Normal Findings
- •7.2.1 Structure
- •7.2.2 Ligaments
- •7.2.3 Hepatic Veins (HV)
- •7.2.4 Portal Vein (PV)
- •7.2.5 Hepatic Artery (HA)
- •7.2.6 Gall Bladder
- •7.2.8 Intrahepatic Bile Ducts
- •7.2.9 Doppler Findings
- •7.2.9.1 Hepatic Veins (HV)
- •7.2.9.2 Portal Vein (PV)
- •7.2.9.3 Hepatic Artery (HA)
- •7.2.10 Special Aspects of Newborns and Infants
- •7.3 Pathology of the Liver
- •7.3.1 Congenital Changes and Normal Variance
- •7.3.1.1 Situs Inversus (Abdominalis)
- •7.3.1.2 Butterfly or Midline Liver
- •7.3.1.3 Hypoplasia/Atrophy of Left Liver Lobe and Other Variations
- •7.3.2 Inflammatory Conditions
- •7.3.2.1 Hepatitis
- •7.3.2.2 Liver Abscess
- •7.3.2.3 Granulomatous Disease
- •7.3.2.4 Role of US
- •7.3.3 Other Parenchymal Liver Disease
- •7.3.3.1 Hepatopathy
- •Fatty Liver/Steatosis
- •Liver Congestion
- •7.3.3.2 Liver Fibrosis
- •7.3.3.3 Cirrhotic Liver
- •7.3.3.4 Liver Involvement in Systemic Disease
- •Cystic fibrosis
- •Glycogen storage disease
- •Tyrosinaemia
- •Wilson disease
- •α1-antitrypsin deficiency
- •Haemosiderosis
- •7.3.3.5 Role of US
- •7.3.4 Portal Hypertension and Vascular Problems
- •7.3.4.1 Portal Hypertension
- •7.3.4.2 Vascular Malformations
- •7.3.4.3 Portal vein and hepatic artery stenosis
- •7.3.4.5 Hepatic vein thrombosis/occlusion/stenosis
- •Budd-Chiari syndrome
- •Veno-occlusive disease (VOD)
- •Increased right atrial/intrathoracic pressure
- •7.3.4.6 Portosystemic Shunts
- •7.3.5 Liver Trauma
- •7.3.5.1 Liver Haematoma
- •7.3.5.2 Contusion
- •7.3.5.3 Laceration
- •7.3.5.4 Haemobilia
- •7.3.5.5 Associated Diaphragmatic Injury
- •7.3.5.6 Liver Infarction
- •7.3.5.7 Role of US in Liver Trauma
- •7.3.5.8 Additional Imaging
- •7.3.6 Space-Occupying Liver Lesions
- •7.3.6.1 Simple Cysts
- •7.3.6.2 Complicated Cysts
- •7.3.6.3 Liver Calcifications
- •7.3.6.4 Intrahepatic Gas
- •7.3.6.5 Haemangioma
- •7.3.6.6 Mesenchymal Hamartoma
- •7.3.6.7 Focal Nodular Hyperplasia (FNH)
- •7.3.6.8 Hepatic Adenoma
- •7.3.6.9 Fatty Tumours
- •7.3.6.10 Hepatoblastoma
- •7.3.6.11 Hepatocellular Carcinoma
- •7.3.6.12 Hepatic Sarcomas
- •Embryonal Cell Sarcoma
- •Rhabdomyosarcoma
- •Angiosarcoma
- •Hepatic Leiomyosarcoma
- •7.3.6.13 Metastasis
- •7.3.6.14 Proliferative Disorders
- •7.3.6.15 Role of US
- •7.3.6.16 Additional Imaging
- •7.4 Biliary Tract and Gall Bladder
- •7.4.1 General Findings
- •7.4.2 Congenital Conditions and Normal Variants of Biliary Tract
- •7.4.2.1 Intrahepatic Gall Bladder
- •7.4.2.3 Choledochal cyst
- •7.4.3 Biliary Tract Diseases
- •7.4.3.1 Aerobilia
- •7.4.3.2 Cholestatic Changes/Inspissated Bile/Gall \stone
- •7.4.3.3 Sclerosing cholangitis
- •7.4.3.4 Other Forms of Cholangitis and Cholecystitis
- •7.4.4 Tumour-Like Conditions
- •7.4.4.1 Polyps
- •7.4.4.2 Tumours
- •Cholangiocellular Tumours
- •Granular Cell Tumour
- •7.4.5 Role of US
- •7.4.5.1 Cholestasis and Jaundice
- •7.4.5.2 Malformations
- •7.4.5.3 Trauma
- •7.4.5.4 Postoperative Conditions
- •7.4.5.5 Metabolic Disease
- •7.4.7 Additional Imaging
- •7.5 US in Liver Transplantation
- •7.5.1 Pretransplant US
- •7.5.1.1 Recipient Evaluation
- •7.5.2 Intraoperative US
- •7.5.3 Postoperative Assessment
- •7.5.4 Typical Complications
- •8: Spleen and Pancreas
- •8.1 Spleen
- •8.1.1 Requisites
- •8.1.2 Positioning
- •8.1.3 Indications
- •8.1.4 Course of Investigation
- •8.1.5 Normal Anatomy
- •8.1.6 Normal Variants
- •8.1.6.1 Splenunculus (Accessory Spleen)
- •8.1.6.2 Splenic Lobulations and Clefts
- •8.1.7 Malformations
- •8.1.7.1 Asplenia
- •8.1.7.2 Polysplenia Syndrome
- •8.1.7.3 Wandering Spleen
- •8.1.8 Splenomegaly
- •8.1.9 Trauma
- •8.1.10 Splenic Infarction
- •8.1.11 Space-Occupying Lesions of the Spleen
- •8.1.11.1 Cysts
- •8.1.11.2 Abscess
- •8.1.11.3 Tumours and Space-Occupying Lesions
- •8.1.11.4 Role of US
- •8.2 Pancreas
- •8.2.1 Requisites
- •8.2.2 Indication
- •8.2.3 Course of Investigation
- •8.2.4 Normal Findings
- •8.2.5 Variations and Malformations
- •8.2.5.1 Annular Pancreas
- •8.2.5.2 Pancreas Divisum
- •8.2.6 Inflammation: Pancreatitis
- •8.2.6.1 Oedematous or Reactive Pancreatitis
- •8.2.6.2 Haemorrhagic or Necrotising Pancreatitis
- •8.2.6.3 Chronic Pancreatitis
- •8.2.7 Trauma
- •8.2.8 Space-Occupying Lesions
- •8.2.8.1 Cysts/Pseudocysts
- •8.2.8.2 Tumours
- •8.2.9 Role of US
- •8.2.10 Additional Imaging
- •8.3.1 Abdominal Vessels
- •8.3.1.1 Positioning
- •8.3.1.2 Transducers
- •8.3.1.3 How to Investigate
- •8.3.1.4 US Findings
- •8.3.1.5 Important Variants and Malformations
- •8.3.2 Vascular Pathology
- •8.3.2.1 Thrombosis/Occlusion
- •8.3.2.2 Pelvic Congestion Syndrome
- •8.3.2.3 Mid-aortic Syndrome
- •8.3.2.4 Retroaortic Left Renal Vein: Nutcracker Syndrome (see Chap. 10)
- •8.3.2.6 Arteriosclerotic Changes and Aneurysms
- •8.3.2.7 Embolic Thrombus to Abdominal Aorta
- •8.3.2.8 Role of US
- •8.3.2.9 Complementing Imaging
- •8.3.3 Mesentery
- •8.3.3.1 Mesenteric (Peritoneal) Masses
- •Cyst
- •Lymphatic Vascular Malformation and Other Tumours
- •8.3.3.2 Abscesses
- •8.3.3.3 Twisted Appendices Epiploica
- •8.3.4 Mesenteric Lymph Nodes
- •8.3.5 Free Intraperitoneal Air
- •8.3.6 Free Intraperitoneal Fluid: Ascites
- •8.3.7 Retroperitoneal Soft Tissues
- •8.3.7.1 Lymph Nodes
- •8.3.7.2 Retroperitoneal Tumours
- •8.3.8 Abdominal Wall
- •9: US of the Gastrointestinal (GI) Tract
- •9.1 Stomach
- •9.1.1 Requisites
- •9.1.2 How to Investigate
- •9.1.2.1 Access
- •9.1.2.2 Functional Assessment of Bowel and Stomach
- •9.1.3 Normal Findings
- •9.1.4 Normal Variants
- •9.1.5 Malformations
- •9.1.5.1 Microgastria
- •9.1.5.2 Pyloric Atresia
- •9.1.5.3 Congenital Hiatal Hernia
- •9.1.6 Pathologic Findings
- •9.1.6.1 Gastro-Oesophageal Reflux (GOER)
- •9.1.6.2 Hypertrophic Pyloric Stenosis (HPS)
- •9.1.6.3 Other Stomach Conditions
- •Gastritis/Ulcers
- •Bezoars and Foreign Bodies
- •Hyperplastic Gastric Mucosa
- •Menetrier’s Disease: Giant Hypertrophy of Gastric Mucosa
- •Eosinophilic Gastr(oenter)itis
- •Gastric Perforation
- •Granulomatous Disease
- •Duplication Cysts
- •Teratoma
- •Focal Foveolar Hyperplasia
- •Inflammatory Pseudotumour
- •Other Benign Tumours
- •Malignant Masses
- •9.1.7 Role of US
- •9.2 Bowel
- •9.2.1 Preparation and Requisites
- •9.2.2 Course of Investigation
- •9.2.3 Normal US Findings
- •9.2.4 Pathology
- •9.2.4.1 Congenital Anomalies
- •Atresia
- •Malrotation
- •Volvulus
- •Hirschsprung Disease/Neuronal Intestinal Dysplasia (NID)
- •Duplication/Diverticula
- •Meckel’s Diverticulum
- •9.2.5 Acquired Obstructive Pathology
- •9.2.5.1 Meconium Ileus
- •9.2.5.2 Midgut Volvulus
- •9.2.5.3 Sigma Volvulus
- •9.2.5.4 Hernia
- •9.2.5.5 Intussusception
- •9.2.5.6 Tumours
- •9.2.6 Inflammatory Conditions
- •9.2.6.1 Necrotising Enterocolitis (NEC)
- •9.2.6.2 Gastroenteritis
- •9.2.6.3 Henoch-Schönlein Purpura
- •9.2.6.4 Appendicitis
- •9.2.6.5 Crohn’s Disease
- •9.2.6.6 Colitis
- •9.2.6.7 Other Inflammatory Bowel Conditions
- •9.2.6.8 Bowel Trauma
- •10: Ultrasound of the Urogenital Tract
- •10.1 Requisites
- •10.1.1 Indications
- •10.1.2 Preparation
- •10.1.3 Transducers
- •10.1.4 Positioning
- •10.1.5 How to Investigate
- •10.1.5.1 Diuretic US
- •10.2 Normal Findings
- •10.2.1 Bladder
- •10.2.2 Kidney
- •10.2.2.1 Normal Variants
- •Duplex Kidney
- •Ectopic Kidneys
- •Renal Agenesis
- •Fusion Anomalies and Other Rare Findings
- •10.3 Pathology of the Kidney
- •10.3.1 Congenital Conditions
- •10.3.1.1 Dysplasia/Hypoplasia
- •10.3.1.2 Cystic Renal Disease
- •Inherited/Congenital Cystic Disease
- •Acquired Cystic Kidney Disease
- •10.3.1.3 Alteration of Urinary Drainage
- •Hydronephrosis (HN)
- •Ureteropelvic Junction Obstruction (UPJO)
- •Uretero-Vesical Junction Obstruction (UVJO)/Obstructive Megaureter (POM/MU)
- •Posterior Urethral Valve (PUV)
- •Vesico-Ureteric Reflux (VUR)
- •Secondary Obstruction
- •10.3.2 Inflammatory Renal Parenchymal Conditions
- •10.3.2.1 Pyelitis
- •10.3.2.2 Acute Pyelonephritis (aPN)/Interstitial Nephritis
- •10.3.2.3 Necrosis and Abscess Formation
- •10.3.2.4 Scarring
- •10.3.2.5 Tuberculosis
- •10.3.2.6 Xanthogranulomatous Pyelonephritis
- •10.3.2.7 Glomerulonephritis/Nephrotic Syndrome
- •10.3.3 Vascular Conditions
- •10.3.3.1 Renal Artery Stenosis
- •10.3.3.2 Arteriovenous Fistula (AVF)
- •10.3.3.3 Infarction
- •10.3.3.4 Renal Vein Thrombosis
- •10.3.4 Nephrocalcinosis
- •10.3.5 Urolithiasis
- •10.3.6 Other Important Renal Parenchymal Disease
- •10.3.6.1 Haemolytic Uremic Syndrome (HUS)
- •10.3.6.2 Glomerulonephritis/Nephrotic Syndrome
- •10.3.6.3 Scars, Cirrhotic Kidney
- •10.3.7 Renal Failure (RF)
- •10.3.8 Renal/Urinary Tract Trauma
- •10.3.9 Renal Tumours
- •10.3.9.1 Benign Tumours
- •10.3.9.2 Pre- or Semimalignant Tumours
- •10.3.9.3 Malignant Tumours
- •10.4 Renal Biopsy and Interventions
- •10.4.1 Renal Biopsy
- •10.4.2 Drainage/Nephrostomy
- •10.4.3 Postoperative Imaging
- •10.4.3.1 After VUR Treatment
- •Cystoscopic Treatment
- •Antireflux Surgery
- •10.4.3.2 Findings After Pyeloplasty
- •10.4.3.3 After Various Interventions
- •10.5 Renal Transplant
- •10.5.1 Normal US Findings in Renal Transplant
- •10.5.2 Pathologic US Findings
- •10.6 Adrenal Glands and Pararenal Space
- •10.6.1 General Remarks
- •10.6.2 Typical Normal US Finding
- •10.6.3 Pathologic Findings
- •10.6.3.1 Adrenal Gland Haemorrhage
- •10.6.3.2 Inflammatory Condition
- •10.6.3.3 Tumours
- •Adrenal Cysts
- •Adrenal Adenoma
- •Neuroblastoma
- •Ganglioneuroma
- •Phaeochromocytoma
- •Adrenal Carcinoma
- •Role of US
- •10.7 US of Urinary Bladder
- •10.7.1 Requisites
- •10.7.2 Pathologic Findings
- •10.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
- •10.7.2.2 Polyps
- •10.7.2.3 Bladder Tumours
- •10.7.2.4 Calcification in/of Bladder
- •10.7.2.5 Ureterocele
- •10.7.2.6 Persisting Urachus
- •10.7.2.7 Megaureter
- •10.7.2.8 Infravesical Obstruction
- •10.7.2.9 Inflammation
- •10.7.2.10 Traumatic Changes
- •10.7.2.11 Vesico-ureteric Reflux
- •10.7.3 Paravesical Changes
- •10.7.3.1 Abscess Formations
- •10.7.3.2 Tumours of Paravesical Region
- •10.7.3.3 Cystic Perivesical Structures
- •10.7.4 Role of US
- •10.8 US of Male Genitals
- •10.8.1 US Technique
- •10.8.2 Normal Findings
- •10.8.3 Common Pathologic Findings
- •10.8.3.1 Hydrocele
- •10.8.3.2 Undescended Testes
- •10.8.3.3 Varicocele
- •10.8.3.4 Cystic Dysplasia of Rete Testis and Seminal Vesicles
- •10.8.3.6 Microlithiasis
- •10.8.4 Inflammation – Orchitis, Ependymitis
- •10.8.5 Scrotal Trauma
- •10.8.6 Torsion
- •10.8.6.1 Torsion of Appendages
- •10.8.6.2 Inguinal Hernia
- •10.8.7 Testicular Tumours
- •10.8.8 Role of US and Additional Imaging
- •10.9 Female Genitals
- •10.9.1 Indications
- •10.9.2 Requisites
- •10.9.3 Transducers
- •10.9.4 How to Perform Investigation
- •10.9.5 Normal Findings
- •10.9.5.1 Sonogenitography
- •10.9.6 Pathologic Findings
- •10.9.6.1 Congenital Malformations
- •Vaginal Septum and Duplications
- •Vaginal Atresia
- •Vaginal Fistula
- •Other Vaginal Malformations
- •Vaginal Aplasia
- •Uterine Malformations
- •Ovarian Malformations
- •10.9.6.2 Inflammatory Conditions of Female Genitalia
- •10.9.6.3 Genital Tumours and Space-Occupying Lesions
- •Cysts
- •Teratoma
- •Other Genital Tumours
- •Rhabdomyosarcoma
- •10.9.6.4 Traumatic Changes
- •Ovarian Torsion
- •Pregnancy
- •10.9.6.6 Role of US/Additional Investigations
- •11: Small Part and Hip Ultrasound
- •11.1 Hip US
- •11.1.1 General Remarks
- •11.1.2 Examination Technique
- •11.1.2.1 Hip US According to Graf
- •11.1.2.2 Modified Graf Classification (Rosendahl)
- •11.1.2.3 Hip US According to Harcke
- •11.1.3 Normal Anatomy
- •11.1.3.1 US Criteria in Graf
- •11.1.3.2 Rosendahl Modification
- •11.1.3.3 Normal Findings During Harcke Investigation
- •11.1.3.5 Hip US in Older Children
- •11.1.4 Pathologic Findings
- •11.1.4.1 Developmental Dysplasia of the Hip (DDH)
- •11.2 Other Conditions of Hip Joint
- •11.2.1 Arthritis and Inflammation of Hip Joint
- •11.2.1.1 Capsular Thickening
- •11.2.1.2 Joint Fluid/Effusion
- •11.2.1.3 Hip Osteoarthritis
- •11.2.3 Perthes Disease
- •11.3 Investigation of Bones, Joints, Tendons
- •11.3.1 Requisites and Technique
- •11.3.2 Typical Normal Findings
- •11.3.3 Pathologic Findings
- •11.3.3.1 Fracture
- •11.3.3.2 Joint Effusion
- •Simple Effusion
- •Complicated Effusion
- •11.3.3.3 Arthritis
- •11.3.3.4 Trauma
- •Haematoma
- •Rupture of Tendon
- •11.3.3.5 Cysts
- •11.3.3.6 Inflammation
- •Myositis
- •Cellulitis
- •Fasciitis
- •Tendinitis – Tendovaginitis/Synovitis
- •Osteomyelitis, Soft Tissue Abscess
- •11.3.3.7 Neoplasia
- •11.3.3.8 Foreign Bodies
- •11.3.3.9 Peripheral Nerves
- •11.4 US for Peripheral Vessels
- •11.5 US-Guided Interventions
- •Index

144
4 Ultrasound of the Neck
Fig. 4.4 Glands and tonsils. Normal parotid gland, note the normal slightly prominent hypoechoic,
nodular-shaped tonsil below the echogenic triangular gland as often observed in infants and children, adjacent normal homogenously echogenic tongue
Fig. 4.5 Larynx US. Normal US appearance of yet non-ossifi ed larynx
4.2.3.4 Para- and Retropharyngeal Spaces
Only meaningfully assessable in case of pathology, such as parapharyngeal abscess
or paravertebral tumour. Otherwise not a routine target of US investigation, retropharyngeal space is diffi cult to visualise.
4.2.3.5 Larynx
Especially in infant/younger children, laryngeal US often diffi cult due to limited
patient cooperation.
Cartilaginous structures nicely assessable – helpful for assessing congenital malformations (e.g. cysts, haemangioma), posttraumatic changes (e.g. haematoma of
vocal cord) and similar queries (Fig. 4.5 ).
NOTE : It is important to know age-dependent anatomic appearance (varies with
progressive calcifi cation).
4.2.4 Cervical Vessels
Normal anatomy with respective US and Doppler fi ndings of major vessels shown
in Fig. 4.1 .

4.2 Normal Findings
145
ab
Fig. 4.6 Cervical vessels. Anatomy + typical US appearance of carotid artery ( a ) using aCDS and
the vertebral artery with accompanying vein ( b ) on CDS (note shadowing from transverse process
of cervical vertebra)
US Findings :
Vessel – anechoic tubular structure
• Artery – multilayered thick wall.
• Vein – usually thin wall, valves may be visible and more easily compressible:
– Veins show signifi cant variation in diameter depending on respiratory cycle
and intrathoracic/transducer pressure – used for assessing patency.
NOTE : Physiologic venous ectasia may be present, particularly during valsalva
manoeuvre.
CDS (Fig.
4.6 )
• In arteries – biphasic unidirectional fl ow towards head.
• In (jugular) veins – usually three-phase modulated fl ow, inspiratory and expira-
tory velocity variations can be bidirectional.
Spectral Analysis
Essential – typical fl ow patterns can be demonstrated in individual arteries (see
4.1 ):
Fig.
• CCA – intermediate resistive fl ow pattern, relatively low antegrade diastolic
velocity and RI = 0.7–0.9.
• ICA – low-resistant fl ow pattern, higher diastolic velocity and RI = 0.6–0.7.
• ECA – fl ow profi le resembles any peripheral high-resistance vessel with low,
potentially missing or inverted end-diastolic fl ow, RI = 0.9–1.1.
• VA – may resemble CCA or ICA fl ow, depending on area of measurement and
head position as well as dominant/nondominant vessel; fl ow velocities usually
slightly lower than CCA; fl ow profi le may change with altered head position
(particularly in fi rst year of life – see Fig.
3.12b–e ).
• All vessels: sharp systolic upstroke, short acceleration time and narrow Doppler
envelope (i.e. narrow band of velocities, no spectral broadening).
• Flow velocities: vary with age (peak systole = 40 cm/s in newborn, 150 cm/s in
adolescents), vessel part and head position (particularly VA).
NOTE : Flow profi le and velocities also depend on many other systemic factors.
Venous fl ow pattern is described above.

146
4 Ultrasound of the Neck
4.3 Pathologic Findings
4.3.1 Lymph Nodes
US Findings
Enlargement, changed echotexture (inhomogenicity, missing hilus, increased or
decreased echogenicity), focal structural alterations (infi ltration, abscess formation), irregular or spherical shape, diameter >1 cm and length-to-diameter ratio
>0.8. Conglomeration, large bulk of nodes, focal large spherical anechoic node,
changed architecture (Fig. 4.7 ).
Potential dorsal enhancement, particularly after anechoic or necrotic parts
NOTE : In enlarged nodes always assess adjacent soft tissue structures and glands
in search for complications or origin (e.g. tumour, secondary abscess formations
in paratonsillar/pharyngeal region). Furthermore, there may be fi stula tracts
(e.g. in MOTT, mycobacteria infection other than tuberculosis, dental origin)
(Fig. 4.8 ).
CDS
For potential disruption of vascular architecture, focal non-perfused areas in granulomatous or tumorous infi ltration/abscess formation (see Fig. 4.2 ).
• In infl ammation hypervascularity and hyperaemia (increased diastolic velocity
with reduced RI).
• 3DUS may be particularly useful for demonstrating disrupted vascular
architecture.
NOTE : Though various criteria indicate suspicion of malignancy, US cannot reli-
ably defi ne entity; some infl ammatory nodes look similar to malignant nodes (e.g.
granulomatous disease), whereas some malignant nodes (e.g. hypervascular lymphoma) may resemble hyperaeremic infl ammatory changes.
4.3.2 Pathology of Cervical Soft Tissue
4.3.2.1 Malformations
Cervical Cyst
Congenital malformation and positioned medially (median cyst – remnant of thyreoglossal duct) or lateral (remnant of embryological branchial arches/clefts).
US Findings
Complicated or simple cyst may contain echogenic debris. May get infected and
then resemble abscess with complicated fl uid, perifocal oedematous changes of
adjacent soft tissue and dorsal sound amplifi cation – but cyst wall is thinner, more
regular and sharper than abscess (Fig. 4.9 ).
Dermoid Cyst
Subcutaneous cyst may contain echogenic material, but no specifi c US criteria.
Duplication Cysts
Arise from trachea or oesophagus (usually lower neck) and may get infected.

4.3 Pathologic Findings
Fig. 4.7 US in lymph node
pathology. ( a ) Split image, sagittal
lateral neck – grouped spherical
enlarged lymph nodes ( LK ). ( b )
Extended fi eld of view, similar
region: a large node (….) with
multiple smaller adjacent
conglomerated lymph nodes
147
a
b
a b
Fig. 4.8 Fistula tact in necrotising node infl ammation/abscess. ( a ) Large suppurated lymph node
with fi stula tract to skin in infection with atypical mycobacteria. ( b ) Fistula tract deriving from
mandibula – from dental infection
ab
Fig. 4.9 Cervical cysts. ( a ) Lateral branchial cleft cyst. ( b ) Median cervical (ductus thyreoglossus)
cyst adjacent to larynx, with clinical signs of secondary infection, dorsal through transmission
cause increased echogenicity behind the complex cyst with sedimentations confi rming its liquid
nature. Note : US alone cannot always differentiate between an old or infl amed cyst/abscess
US Finding
• Cyst-like appearance and may cause compression of adjacent structures.
• Some wall structure (with respective gut/bronchial signature) depictable, often
with complex contents, air within if connection to structure of origin.

148
4 Ultrasound of the Neck
ab
Fig. 4.10 Cervical thymus. ( a ) Cervical ectopic thymus adjacent to thyroid gland. No connection
to mediastinum. ( b ) Large neonatal thymus that reaches up into lower median cervical space
Thymic Cyst
Positioned (para-)median, inferior to thyroid gland, on entire pathway down to
mediastinum.
Vary in size, otherwise undistinguishable from any other uncomplicated cyst.
Cervical Ectopic Thymus
Either isolated or connected to thymus, resembling typical thymal echotexture (see
Chap. 6 ) (Fig. 4.10 ). Intermittent cervical herniation of thoracic thymus may occur
with crying or valsalva.
4.3.2.2 Tumours
Haemangioma
Cavernous or capillary haemangioma, positioned superfi cially and show typical
skin discolouration.
US Findings
• Depending on anatomy and entity, more or less homogeneous, echogenic,
tumour-like lesions, potentially with hazy margins and some infi ltrating aspects
and tubular anechoic structures (representing dilated vessels).
• Central thrombosis may be present (Fig. 4.11 , also see Chap. 11 ).
CDS
• Hyperaemia and hypervascularisation.
• Often some major feeding vessels can be depicted.
Spectral Analysis
• Differentiates lesions into high- and low-fl ow vascular or arterial/venous malfor-
mations; arteriovenous shunts can be identifi ed.
NOTE : Same phenomena and classifi cation/imaging appearance as anywhere else
in body.
Lymphatic Malformation
US Findings
• Mass of septated cysts, potentially with some nodular tissue.
• Tend to bleed – then show mixed echogenicity, sometimes with fl uid-fl uid levels
(see also Chap. 11 ) (Fig. 4.12 ).
aCDS
• Potentially some high-resistance vessels within septae.

4.3 Pathologic Findings
Fig. 4.11 Cervical masses –
haemangioma. ( a ) Gray scale
image shows nonspecifi c
echogenic, well-demarked mass
below an area with only minor
skin discoloration, as the
tumour is mainly positioned
subcutaneously. ( b ) CDS shows
hypervascularisation – consistent
with a haemangioma
149
a
b
ab
Fig. 4.12 Cervical cystic lymphatic malformation. ( a ) Gray scale image of a cystic “lymphangi-
oma” (lymphatic vascular malformation) with central complex cyst that exhibits echoes with fl uid
levels and sedimentation after haemorrhage. ( b ) aCDS demonstrates vascularised septae without
any fl ow in cystic parts
NOTE : Often mixed tumours (containing haemangiomatous and lymphangioma-
tous as well as other mesenchymal tissue) can be encountered; defi nite differentiation only by histology. Look similar everywhere in the body.
Other Mesenchymal Tumours
Various tumours: lipoma, fi broma, fi brolipoma and sarcomatous variants
US Findings
• No specifi c US features.
• Aggressive fi bromatosis more invasive, infi ltration with destruction of borders
and may exhibit inhomogenous echogenicity.
NOTE : Same appearance as everywhere else.

150
4 Ultrasound of the Neck
Neuroblastoma, (Ganglio-)Neuroma, Neurofibroma and Other Nerve (Sheath) Tumours
See respective chapters, defi nitive diagnosis of entity often requires histology.
NOTE : Neuroblastoma tends to invade spinal canal, particularly in the neck, and
may have calcifi cations.
Teratoma
US Findings
• US appearance varies with its components. May be purely cystic or may have
fatty or calcifi ed compartments, with more or less large solid components.
• Same appearance as everywhere else.
• Details discussed with genital tumours (see Chap. 10 ).
Other Malignant Tumours
Commonly rhabdomyosarcoma, but also liposarcoma, metastases and lymphoma.
US Findings
• Usually tumour depictable.
• Sometimes origin and affected space can be defi ned.
Diagnosis usually by histology.
NOTE : Imaging appearance varies – specifi c diagnosis of underlying entity often
impossible.
Role of US
Shows lesion, defi nes relation to surrounding structures, potentially guides biopsy
and serves for follow-up.
4.3.2.3 Abscess Formations
All infl ammatory changes may also manifest in neck, resembling fi ndings in other
body compartments (cellulitis/phlegmon, abscess).
US Findings
Originates from phlegmonous soft tissue (increased echogenicity of swollen tissue
with more or less fl uid collections, particularly along septae, hypervascularisation –
may also be seen around abscess) or other infl ammatory conditions.
Abscess formation – central complex fl uid with fl oating echoes and dorsal
through transmission, surrounding membrane-like abscess wall with perifocal
infl ammatory changes (Fig. 4.13 ).
CDS
• Hypervascular wall (no vessels in central necrotic part).
• Potentially secondary vascular involvement – particularly of jugular vein –
always includes assessment of ipsilateral, particularly venous, structures.
NOTE : US insuffi cient for deeply located abscesses, cannot exactly defi ne anatomy
and extension (e.g. mediastinal or skull-base extension) – additional cross- sectional
imaging advisable especially preoperatively. Differentiation of primary abscess
from infected pre-existing cystic formation (cervical cyst, lymphatic malformation)
sometimes impossible/diffi cult.

4.3 Pathologic Findings
151
a
b
c
Fig 4.13 Cervical abscess. ( a ) Gray scale image of a complex cystic mass with fl uid levels and
debris (+ +) – together with the clinical fi ndings consistent with an abscess. ( b ) CDS: vascularised
capsule, no central vessels and compression of adjacent vein in a superfi cial lymph node abscess.
( c ) CDS, axial section: abscess (+ +) of the deeper parapharyngeal space
All abscesses, e.g. from lymph nodes, tonsils and other soft tissues, exhibit no
other imaging criteria than mentioned above and have same appearance everywhere
else in the body.
4.3.2.4 Traumatic Changes
Haematoma (Including Sternocleidomastoid Muscle “Haematoma”)
US Findings
• Initially echogenic, later hypoechoic, potentially inhomogenous.
• May eventually develop into cyst-like appearance (seroma).
• Typically seen in muscles as well as subcutaneously, rarely in larynx.
• May be diffi cult to differentiate perifocal (reactive) changes/swelling from
haematoma.
NOTE : The typical sternocleidomastoid muscle “ haematoma ” in newborns with resul-
tant torticollis – usually after birth trauma, also called/consistent with benign fi broma-
tosis colli of unclear origin resulting from contracture of muscle – can be identifi ed as
fusiform sternocleidomastoid muscle enlargement in continuity within fascial and
muscle borders. Echogenicity may vary depending on age and insonation angle (from

152
4 Ultrasound of the Neck
a b
c
Fig. 4.14 US images of a fi bromatosis colli. ( a ) Oblique section, preserved muscle structure and
septae (+ +). ( b ) Large tumour-like appearance – the entire length only depictable by extended
view US (+ +) may sometimes be huge and frightening; however, other imaging has no higher
specifi city, biopsy not indicated. ( c ) Typical confi guration aligning along the fascia of the sterno-
cleidomastoid muscle
hypoechoic to slightly hyperechoic) (Fig. 4.14 ). Sometimes typical muscular septae
preserved. Small calcifi cations occur hypervascularisation may be present on CDS.
NOTE : Does not need (additional) imaging; do not mistake for rhabdomyoma,
aggressive fi bromatosis and other (malignant) tumours.
4.3.3 Thyroid Gland
4.3.3.1 Cystic Changes
Cysts may be normal and may be congenital, posttraumatic or regressive cysts – the
latter after/in thyroid disease. Many focal, partially cystic lesions exist – for a DDx
list, see Table 4.1 .
US Findings
• Anechoic spaces with thin membrane and sharp borders.
• If proteinaceous component, secondary haemorrhage or infection – fl oating
echoes.
• Can be differentiated from nodular solid lesions by typical dorsal through trans-
mission and no vessels on aCDS.
4.3.3.2 Malformations
Typical query in newborn: is there (ectopic) thyroid tissue?
• Gland may be hypoplastic or hypertrophic, asymmetric, etc. – numerous form
and shape variations. (Fig. 4.15 ).
• Size does not necessarily correspond with function.

4.3 Pathologic Findings
153
a
c
Fig. 4.15 Thyroid shape and position variations. ( a ) Thyroid agenesis – no thyroid tissue depict-
able. ( b ) Ectopic thyroid situated at base of tongue (+ +). ( c ) Only one single, but hypertrophic
thyroid lobe – the left lobe is absent
b
4.3.3.3 Inflammation
Either focal or diffuse. Typically thyroid gland enlarged with slightly altered
echotexture; echogenicity can be increased, sometimes (also focally) decreased –
inhomogenous appearance possible.
US Findings (Fig. 4.16 )
• Subacute thyroiditis: typically anechoic patchy changes.
• Lymphocytic thyroiditis (Hashimoto): more globally patchy anechoic disruption
of echotexture.
• Morbus Basedow/Graves’ disease (hyperthyroidism)/immune processes, pronounced
swelling of isthmus, diffusely swollen and more or less homogeneous gland:
– CDS: signifi cant hypervascularisation (“thyroid inferno”).
• Sclerosing thyroiditis: gland eventually gets smaller, rather inhomogenously
hypoechoic, sharp contours with regional bumpy alterations of surface.
CDS
Hypervascularisation – unspecifi c, in late phases (atrophy) reduced vascularity.
– Corresponds more with function/treatment than underlying entity.
4.3.3.4 Other Conditions
Hypothyroidism/Struma Diffusa/Colloides (Fig. 4.17 )
Slightly enlarged gland with patchy structure, potentially increased echogenicity.
The neonatal goiter with maternal hypothyroidism usually is slightly enlarged and
with only slight hypervascularity; huge goiters and hypervascularity hint towards
(genegtic) thyroid hormon synthesis defects.
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