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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

114
3 Neurosonography in Neonates, Infants and Children
velocities (cause some jet phenomenon, where one may fi nd intermittent undulating jets that vary with respiration or with other forms of increased thoracic
pressure, such as crying, breath hold and ventilation manoeuvres).
NOTE : For any measurements of CSF spaces, standardised approach with repro-
ducible measurements should be applied; CSF overdrainage can cause ventricular
collapse and secondary subdural haemorrhage/effusion which may clinically mimic
shunt dysfunction and increased brain pressure.
• 3DUS particularly valuable: complete documentation, reproducible measurement
at comparable section and comparison to other sectional imaging (any desired
section may be reconstructed from 3DUS data set) (Figs. 3.34c , 1.26 , and 1.27 ).
3.3.8 Cerebral Haemorrhage
Various forms of haemorrhage need to be differentiated in terms of location and
aetiology: intra- and extracranial, intra- or extraventricular, parenchymal, extracerebral (sub-galeal haematoma, subcutaneous haematoma, subdural, epidural, subarachnoid, etc.). etc. (Fig. 3.35 ). Type of haemorrhage varies with age: preterms
have different haemorrhages than term neonates or infants.
3.3.8.1 Haemorrhage in Preterm Babies – IVH Grades I
to III, PVH (Fig.
3.36 )
Typically occur in germinal matrix near head of caudate nucleus, where immature
vessels tend to rupture with only mild trauma, unstable blood pressure and intravascular volume changes, etc.
IVH I : on US echogenic round or oval-shaped area below plexus and head of
caudate nucleus (intraventricular haemorrhage grade I = IVH I ) – to be differentiated
from swollen choroid plexus (also echogenic, but usually entire plexus affected) or
choroid plexus bleeds (occur at any location of plexus, but commonly close to
a b
Fig. 3.35 Scheme: cranial haemorrhages. Typical extra- ( a ) and intracranial ( b ) haemorrhages –
site and respective appearance. Abbreviations: SEB/SEH sebependymal bleed/haemorrhage, EDH
epidural haematoma, SDH subdural haematoma, ICH intracerebral haemorrhage, IVH intra–ven-
tricular haemorrhage, SAH subarachnoid haemorrhage and PVH periventricular haemorrhage

3.3 Pathologic Findings
115
a
b
f
Fig. 3.36 Images and schematic drawings demonstrating classifi cation and image appearance of
brain (intra-ventricular) haemorrhage in preterms. ( a ) Scheme plexus bleed and IVH grade I° (sub-
ependymal bleed/haemorrhage = SEB/SEH ), IVH intraventricular haemorrhage. ( b ) Parasagittal
view: IVH I°/SEB, clot seen as somewhat echogenic nodular structure (may be diffi cult to differentiate from plexus haemorrhage). ( c ) Scheme IVH grade II°, III° and IVH + periventricular haem-
orrhage (=PVH, older term IHV IV°). ( d ) Parasagittal view: IVH II°, huge clot in the plexus, a little
bit of blood in the posterior horn. ( e ) Coronal view: fresh haemorrhage with blood fi lling the entire
ventricle lumen = IVH grade III°. ( f , g ) Coronal view: haemorrhage with periventricular haemor-
rhagic infarction/PVH on right ( f ) or left ( g ) (+ +) side
c
d
e
g
frontal attachment, located within plexus). For differentiation – axial section or
axial 3DUS reconstruction helpful.
IVH II : if grade I haemorrhage increases, it ruptures into ventricle – some blood
seen in ventricle (grade II haemorrhage). Initially ventricles not dilated, only little
blood or some clotting in ventricle.
IVH III : with progression of haemorrhage ventricles get dilated, increasingly
fi lled with blood (grade III haemorrhage) Blood also seen in third and fourth

116
3 Neurosonography in Neonates, Infants and Children
a
c
Fig. 3.37 Examples for other cerebral haemorrhages and DDx. ( a , b ) Basal ganglia haemorrhage
(echogenic mass) in term infant ( a ) coronal and ( b ) (para-)sagittal section. ( c , d ) DDx in haemor-
rhage: Echogenic swollen plexus ( b , sagittal section) with hypervascularity on CDS ( c , coronal
view) in a plexus papilloma
b
d
ventricle due to physiological CSF drainage pathways. Due to dilatation of ventricle
paraventricular draining veins get compressed/obstructed/congested – cause venous
infarction of periventricular respective areas ⇨ haemorrhagic infarction.
IVH III + PVH : combination of periventricular haemorrhagic infarction with
grade III haemorrhage (initially called type IV haemorrhage, now classifi ed as
haemorrhage grade III + periventricular haemorrhage = PVH) – attributing new
insight into aetiology and pathophysiology.
3.3.8.2 Haemorrhage in Term Infants
Much rarer, usually do not occur as IVH but as intraparenchymal haemorrhages
(intracerebral haemorrhage – ICH).
Typical locations: basal ganglia and locations of haemorrhagic venous infarc-
tions (Fig. 3.37 ).
Rare other causes that defi ne locations – secondary haemorrhage into hypoxic areas
or trauma:
• Epidural haemorrhages – EDH (e.g. after forceps delivery or skull fractures), use
TCI (Fig. 3.38 ).

3.3 Pathologic Findings
Fig. 3.38 Epidural haemorrhage (+ +). Axial
view – TCI, magnifi ed section: subcalvarian complex
ovaloid fl uid space-occupying lesion in terms of
a subacute EDH
117
a
Fig. 3.39 Tentorial and cerebellar haemorrhage. ( a ) Coronal section, linear transducer: tentorial
and cerebellar haemorrhage. ( b ) Same patient as in ( a ) tilted mastoid-axial view: superior demon-
stration of bleed
b
• Subdural haemorrhages – SDH (consider shaken baby syndrome), linear transducer and TCI helpful (Figs. 3.29 and 3.20d ).
• Subarachnoid haemorrhages – diffi cult to see on US unless large.
• Tentorial bleeds (e.g. after complicated fetal repositioning manoeuvres or breach
delivery) (Fig. 3.39 ).
• Direct impact (trauma), by caesarean section (e.g. cutting too deep, thus injuring
brain through fontanel).
NOTE : Unexplained haemorrhages in neonates and young infants raise suspicion
of nonaccidental injury (NAI) – thorough workup.
US Appearance
All haemorrhages have similar US appearance and development:
• Hyperacute state: blood has similar echogenicity as surrounding tissue – not
seen.
• (Sub)acute state: bright echogenic spot.
• Further course – sedimentation and resorption: inhomogenous with some
hyperechoic areas and clot formation – usually inhomogenously echogenic,
tumour- like areas (Fig.
3.40 ).

118
3 Neurosonography in Neonates, Infants and Children
a
Fig. 3.40 Clot and hydrocephalus after IVH III. ( a ) Coronal section demonstrating inhomoge-
nously echogenic masses within lateral ventricles obstructing foramen of Monro. ( b ) Parasagittal
view: demonstrates clots in dilated lateral ventricle after IVH III
b
• Eventually resorbed – cystic remnants, hyperechoic ventricular wall and parenchymal defects (Fig. 3.20 ).
• Impairment of CSF circulation may cause hydrocephalus – careful monitoring
and assess need for CSF drainage:
– Early phase: drainage sometimes achievable by repeated lumbar punctures.
– Later phases: external drainage and shunt placement necessary.
NOTE : Every term neonate and young infants with haemorrhage may suffer from
rare underlying disease, e.g. coagulopathies, venous thrombosis, vascular anomalies, underlying tumours, hyperviscosity, hypoxia, ischemia, dehydration, septicaemia and meningoencephalitis. Differentiation by US often diffi cult or impossible
(e.g. haemorrhagic infarction diffi cult to differentiate from haemorrhage without
underlying infarction).
3.3.8.3 Role of CDS in Neonatal Haemorrhage
Doppler and CDS does not help in defi ning aetiology or predicting haemorrhage,
however, reduced fl ow velocities and large fl uctuation of fl ow spectra with repeated
examinations (due to lack of autoregulation) associated with higher risk of
haemorrhage:
• Only in severe active bleeding is increased particularly diastolic fl ow with
reduced RI seen in feeding vessel.
• Sometimes CDS depicts vascular anomaly that caused haemorrhage.
• CDS helpful for depiction of thrombosis of large venous pathways.
• aCDS is helpful to differentiate swollen choroid plexus (with existing perfusion)
from choroid plexus bleed or clot.
3.3.8.4 Haemorrhage in Infants and Older Children
After fontanel closure and increasing skull ossifi cation, US possibilities decrease;
particularly detailed assessment of small changes or exclusion of haemorrhage
becomes increasingly diffi cult and eventually impossible. CT and MRI are
mandatory.

3.3 Pathologic Findings
119
a
Fig. 3.41 US for skull fracture. ( a ) Linear transducer: skull fracture sees as disruption of skull
echo. ( b ) Linear transducer: skull fracture with subacute haematoma
b
US Findings :
• Haemorrhage as in transfontanellar view – initially echogenic, relatively sharp
margins.
• As long as US access and penetration possible, large parenchymal bleeds and
large SDH/EDH can be depicted, particularly if cause some mass effect and distort ventricles or midline structures.
NOTE : Do not mistake repeating echoes from (contralateral) skull on transtempo-
ral images for haemorrhage.
• SDH may be recurrent – thus septae develop, with different echogenicity in various compartments. If chronic – hygroma.
NOTE : Usually brain surface fl attened and sulci narrow in area of haematoma – in
atrophy sulci enlarged without fl attening of brain surface. If SDH of different age
always think of NAI, try to assess near-fi eld cortex for depiction of typical teardrop
lesion (resorbed focal venous infarctions) in (sub)cortical area – may be missed if
only sector array used (Fig. 3.20 ).
• Cerebellar and tentorial haemorrhages rare, also bleeds of brain stem and other
posterior fossa structures. Diffi cult for US once skull ossifi ed. Usually have poor
prognosis.
• Transmastoid, -occipital and -temporal access mandatory when evaluating these
potential pathologies.
NOTE : In older children with appropriate history or symptoms, emergency imag-
ing by CT and/or MRI indicated.
• Helpful application: assessment of skull and galea by high-resolution linear
transducers. Haematoma seen, formation of seroma can be documented and
measured, skull fractures – even if only subtle – usually nicely depicted by showing disruption of skull surface echo (Fig. 3.41 ).
• Skull US also helpful for assessment of other skull or skin lesions; e.g. epithelial
cysts, histiocytosis, eosinophelic granuloma, metastases and in some places also
applied for assessment of craniosynostosis.
3.3.9 Tumours and Space-Occupying Lesions
Intracranial tumours represent 15 % of childhood tumours, most occurring beyond
fi rst year of life – therefore not ideally suitable for US diagnosis; in these ages

120
3 Neurosonography in Neonates, Infants and Children
Fig. 3.42 US appearance in a typical neonatal cerebral AVM – ectatic/aneurysmal vein of Galen
malformation. Midline sagittal view: large cystic formation fi lled with fl oating echoes – vein of
Galen malformation
only large tumours depicted particularly if they cause midline shift or
hydrocephalus:
• In infancy mostly teratoma, craniopharyngioma, medulloblastoma/PNET, choroid plexus papilloma and lipoma.
• Older children – larger variety of different tumours.
US Findings :
Tumour echogenicity and texture – nonspecifi c: homogeneous or heterogeneous,
cystic or necrotic areas, haemorrhage and may contain calcifi cations (only large
calcifi cations cause acoustic shadowing).
Secondary signs – consequences of space-occupying lesions – shift/compression
of surrounding structures, compression of ventricle and hydrocephalus.
Some specifi c appearances:
• Echogenic tumour typically in midline – rather specifi c for (callosal) lipoma.
• Choroid plexus papilloma – homogenously echogenic, within plexus, inhomogenous tumours may represent carcinoma; very vascular – CDS is helpful.
NOTE : Additional imaging by preferably MRI or – if not available – CT.
3.3.9.1 Vascular Malformations
Diffi cult to depict on US, particularly beyond fi rst months of life, contrast-enhanced
CDS may increase US potential.
Typical entity – phakomatosis (e.g. Klippel-Trénauny syndrome, Von Hippel-
Lindau syndrome and Bourneville-Pringle disease), tubers and gliomas manifest in
more central portions or at ventricular margins – more easily depicted than common
peripheral or meningeal lesions (particularly venous ectasia with calcifi cation and
thrombosis) as in Klippel-Trénauny, and easily missed → contrast-enhanced MRI.
US Appearance :
• Echogenic – if consisting of many small vessels.
• Tubular or cystic – if consisting of larger vessels and aneurysmal vascular portions (Fig. 3.42 ).
• Show vivid Doppler fl ow only with large or high fl ow shunts: feeding and draining vessels depictable.

3.3 Pathologic Findings
121
a
b
cd
Fig. 3.43 CDS in cranial and cerebral AVM. ( a ) Axial view by TCI-CD: fl ow in aneurysmatic
portion of a vein of Galen malformation, some feeding arteries seen as well as the enlarged draining vein (with high and turbulent fl ow causing aliasing). ( b , c ) Focal mass suspected to be a skin
haemangioma on the skull; CDS demonstrates vivid vascularisation. NOTE: Mirror image artefact
both on gray scale as well as on CDS caused by the highly refl ective skull bone. ( d ) Superior sinus
thrombosis, sagittal view: CDS demonstrates lack fl ow in the superior sagittal sinus which is also
somewhat inhomogenously echogenic; consequently dilated extra-axial CSF space
• Purely venous malformations have low fl ow – diffi cult to depict, particularly on
transcranial imaging.
• Ce-US may improve differentiation from other lesions.
aCDS : helpful particularly in neonates and young infants for :
• Vascular pathology: malformations and aneurysms (intra- and extracranial):
– Particularly typical arteriovenous malformation/fi stula of vein of Galen
(Figs. 3.43a–c and 1.15 ).
NOTE : In vascular malformations, CDS can be misleading, particularly after haem-
orrhage or with thrombotic components, often differentiation from tumours and
other mass lesions impossible.
• Venous thrombosis – poor insonation angle and low fl ow may impair conventional CDS potential (Fig. 3.43d ).
• Signifi cantly hyperperfused tumours (e.g. plexus papilloma – see Fig.
3.37d ):
– Otherwise aCDS not particularly useful for cerebral tumours.
– Potentially for DDx of necrotic parts or compartments containing compli-
cated fl uid (e.g. abscess).
CDS in older children : to some extent transcranial ce-CDS may improve sonographic
potential in depicting vascular malformations or differentiating clots, necrotic areas
or haemorrhages and subacute infarctions from tumours. Atypical fl ow patterns may
indicate shunt fl ow and allow rough estimation of hemodynamics.

122
3 Neurosonography in Neonates, Infants and Children
3.3.10 Cerebral Calcifications
Introduction
Various causes: prenatal infection, peri- and postnatal meningitis, vascular malformations, posthaemorrhagic, neoplastic, phakomatoses, postthrombotic, etc.
Localisation :
• Commonly in supratentorial brain, mostly in basal ganglia and also
hemispheres.
• Commonly in vicinity of vessels and in choroid plexus.
• Calcifi cation-like echoes in cysts or abscess-like formations – suspicion for
parasitic or fungal infection, if in cyst wall – hint at unusual origin (infectious,
posthaemorrhagic, tumorous, etc.).
NOTE : Meningeal calcifi cations diffi cult to depict on US.
US Findings (see Fig. 3.27a ):
• Usually echogenic formations with sharp borders can be scattered and may vary
in size and echogenicity.
• Small calcifi cations lack typical acoustic shadowing.
• Differential diagnosis of calcifi cations diffi cult by US:
– Aetiology can only be assumed in combination with other imaging and par-
ticularly clinical information.
3.3.10.1 Non-calcifying Vasculopathy
(Lenticulostriate Vasculopathy)
Band-like echogenic stripes along vessels, mostly in the basal ganglia (see
Fig. 3.27b ).
3.4 Ultrasound of the Skull
3.4.1 Introduction
US can be used for assessment of subcutaneous pathology as well as disruption of
skull surface.
Always use linear high-resolution high-frequency transducer and plenty US
gel.
3.4.2 Haematoma
Types of haematoma – see Fig. 3.36 . US helpful in differentiating entity:
• Echogenicity and US appearance may help estimate age:
– Acute bleed – rather hyperechoic.
– Older bleed – hypoechoic with sedimentation.
– Chronic bleed or remnants/seroma – anechoic, capsule formation.

3.5 Additional Imaging
123
3.4.3 Space-Occupying Lesions and Tumours
US – resembles fi nding in other small parts (see respective chapter), may visualise
cysts, tumours, metastases, etc.
3.4.4 Skull Fracture
• US depicts disruption of echogenic calvarial bone surface – helpful for assessing
suspicious fi ndings on plain fi lm (Fig. 3.41 ).
• US may help analyse amount of displacement.
• US may help in follow-up – e.g. if growing fracture suspected.
US used to assess sutures and their ossifi cation + differentiating sutures from
fractures:
• Fracture – typically sharp border.
• Suture – dentates shape of borders, similar to plain fi lm; US also used to assess
craniosynostosis in some places.
• 3DUS with surface rendering helpful for differentiation, conspicuously visual-
ises shape of fracture (Fig. 1.33 ) .
3.5 Additional Imaging
3.5.1 Plain Film
Used for visualisation of osseous structures
• Particularly when looking for fractures, calcifi cations, skull defects, skull anom-
alies, etc.
– Dedicated projections used for assessment of premature synostosis.
• Assess continuity of shunt drains.
3.5.2 CT
Indicated for emergency imaging, particularly in older children
• After trauma, suspected haemorrhages and for complicated fractures (always
with surface rendering).
• Hydrocephalus/follow-up after shunt (use specifi c low-dose protocols) – if no
MRI available or contraindicated/unsuitable.
• Stroke (if MRI not available).
• Tumours (if MRI not available).
• CT-Angiography used for vascular assessment:
– Modern volume CT and CT-DSA allow for angiography-like subtraction
images as well as perfusion studies.
NOTE : Considerable radiation burden – try to replace by MRI whenever possible.
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