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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

10.6 Adrenal Glands and Pararenal Space
ab c
Fig. 10.36 Adrenal gland haemorrhage. ( a ) Huge, fresh adrenal gland haemorrhage in a neonate
after birth trauma. ( b ) Same patient as in ( a ): CDS demonstrates normal perfusion of adjacent
kidney (important to check, as adrenal gland haemorrhage can cause/be associated with renal vein
thrombosis); investigation a few days later, with sedimentations due to starting resorption of now
inhomogeneous appearing haematoma. ( c ) Calcifi cation with shadowing of adrenal gland (+ +) – a
remnant of adrenal gland haemorrhage
367
10.6.3.2 Inflammatory Condition
May occur secondarily/haematogenously in systemic disease (e.g. sepsis,
tuberculosis).
US Findings
Unspecifi c enlargement with focal complex fl uid collections in abscess formation:
• Tuberculous abscesses may contain echogenic content, cause calcifi cations.
Tuberculoma is rare.
Eventually diffi cult to differentiate from remnants of adrenal gland haemorrhage.
Role of US
May depict fi ndings; aetiology defi ned by laboratory/clinical fi ndings. US-guided
biopsy?
10.6.3.3 Tumours
Adrenal Cysts
Rare, potentially dysontogenetic, after haemorrhage/infection, tumourous
origin.
US as in any cyst; nonspecifi c, may vary in size:
• Sometimes diffi cult to differentiate from renal cyst/cystic upper pole system.
• May cause focal mass effect, may secondarily cause haemorrhage:
• More complex aspect of cyst may raise suspicion of cystic tumour.
Adrenal Adenoma
Extremely rare in children.
Commonly hormonally active, causing Cushing syndrome/virilisation in girls:
• The latter also associated with diffuse adrenal hyperplasia, diffi cult to identify by
US.
No specifi c US fi ndings.

368
10 Ultrasound of the Urogenital Tract
a
Fig. 10.37 Neuroblastoma. ( a ) Small neonatal neuroblastoma (+ +) – these usually only observed
and often vanish spontaneously; urine catecholamine metabolites tested for proving diagnosis. ( b )
Neuroblastoma (
2
+ +); note still-preserved parts of adrenal gland on left upper aspect adjacent to tumour. ( c )
ment (
Large neuroblastoma in 3-year-old child exhibiting typical calcifi cations and causing mass effect;
thick slab rendering of a 3DUS acquisition enhances those calcifi cation, though inducing some
blurriness
1,3
+ +) in an infant arising from paravertebral ganglia, with regional node involve-
b
c
Neuroblastoma
Most common neonatal tumour, developing from medulla of adrenal gland, may
occur prenatally:
• Low-grade tumours may spontaneously regress/disappear spontaneously, particularly if small.
• Typically associated with elevated catecholamines in urine, however, catecholamine negative variants occur as well as neuroblastoma with other hormonal
activities/respective symptoms.
US / CDS Findings
No specifi c US features that allow diagnosis/differentiation of prognostically varying entities. Commonly ovoid to spherical, space occupying lesion of low echogenicity, sharp margins, stippled echogenic calcifi cations, commonly with only
little shadowing (Fig. 10.37 ):
• Haemorrhage/necrosis possible – appearing like complicated collections/cysts.
• Commonly easily assigned to adrenal gland.
• In large tumours differentiation from exophytic renal/hepatic tumours more challenging – use typical features (e.g. motion during breathing, compression/distortion of adjacent structures).
• CDS may show intratumoural vessels.
• Origin of vessels helpful for differentiating origin of tumour.
• Central vessels help differentiation against haemorrhage, although haemorrhagic
tumours will also not exhibit vasculature in haemorrhagic/necrotic parts.
Staging
Different staging used in different parts of the world, generally performed by sectional imaging; additionally based on histology/surgery fi ndings. Main features:
size, location, resectability/invasion of adjacent organs/structures, focal lymph node
involvement, systemic metastases (particularly liver assessable by US).

10.6 Adrenal Glands and Pararenal Space
369
Fig. 10.38 Other adrenal tumours. ( a ) Enlarged adrenal gland with atypical appearance in adre-
nogenital syndrome/congenital adrenal hyperplasia. ( b ) Adrenal gland tumour in child with severe
hypertension: phaeochromcytoma
a
b
NOTE : Neuroblastomas occur also in other body areas (from neck to pelvis) within
remnants of neurogenic crest – mostly in paravertebral ganglia. In these less- typical
locations more diffi cult to depict (in suspected neuroblastoma actively search all
these locations). Tend to invade neuroforamina/spinal canal, displace/encase retroperitoneal vessels (see Fig. 8.27c ).
Ganglioneuroma
Usually occurs in paravertebral ganglia, more benign variant of neuroblastoma, not
distinguishable by US (Fig. 10.36 ).
Phaeochromocytoma
Rare tumour in infancy/childhood, arising from adrenal medulla/sympathetic paravertebral or paraaortal ganglia (neck to pelvis). Typically associated with elevated
blood pressure/respective hormonal fi ndings.
May be familial/combined with other entities (e.g. sarcomatosis, multiple endo-
crine neoplasia and bilateral manifestation).
US Findings
Well-defi ned tumour with sharp borders, sometimes somewhat inhomogeneous,
intermediate echogenicity. Parenchymal calcifi cations/areas of increased echogenicity are possible (Fig.
10.38 ).
NOTE : Entity not defi ned by US but by associated clinical symptoms/hormonal
(laboratory) fi ndings.
Adrenal Carcinoma
Extremely rare in childhood, very aggressive, arises from cortex, may be hormonally
active.

370
10 Ultrasound of the Urogenital Tract
US Findings
Usually hypoechoic, more or less homogenous, aggressive mass infi ltrating surrounding structures, even penetrating diaphragm/into pleural space (see Fig. 6.9 ).
Early metastases locally/systemically, may invade vessels. No specifi c other signs.
Role of US
Screening method in all conditions with potential adrenal gland involvement, such
as hormonal symptoms, virilisation, precocious puberty, adrenogenital syndrome,
signs of acute haemorrhage (e.g. after asphyxia, unexplained neonatal anaemia) and
hypertension.
Furthermore used for follow-up.
For DDx/tumour staging, sectional imaging mandatory; in neuroblastoma
include MIBG scintigraphy. Always search for tumour-specifi c metabolites in urine
and blood (catecholamines).
10.7 US of Urinary Bladder
10.7.1 Requisites
Suffi cient bladder fi lling is essential:
• If not achievable by drinking, consider catheterisation with instillation of saline.
• For assessing potential VUR, additional instillation of US-CM feasible (ce-VUS;
see Chap. 2 ).
NOTE : Always assess before and after voiding; consider US during voiding using
perineal transducer position for urethral assessment. Always include paravesical
space/collecting system of both kidneys before/after voiding.
Transducers
Commonly curved linear arrays used – also for detailed assessment of urethra during
voiding (perineal US), measurement of bladder wall; linear transducers are also used:
• Diffi cult access: small footprint sector transducer may be an option.
• Neonates/infants: (additionally) high-resolution linear transducer, particularly
also for urachus assessment.
How to Assess
Always assess bladder in longitudinal and transverse sections (see Fig. 10.1 ):
• Oblique sections through area of ostium (used to visualise distal/transmural
ureters).
Actively evaluate trigone, bladder neck, ostium, bladder wall and bladder roof (urachal remnants):
• Include paravesical space (internal genitalia, ascites, etc.).
If possible/indicated: add perineal sagittal sections for urethra (vagina)
visualisation:
• Bladder wall measurements should always be taken in suffi ciently full bladder,
never at trigone; should generally not exceed 2 mm in full bladder (otherwise
cut-off = 4 mm).

10.7 US of Urinary Bladder
371
a
b
cd
Fig. 10.39 Bladder pathology. ( a ) Trabeculation of bladder wall in a neurogenic bladder. ( b , c )
Small ( b ) and large (c,
increased intravesical pressure (same patient as c ) causing aberrant voiding
1
+....+) diverticulum. ( d ) CDS shows urine infl ux into diverticulum with
• Bladder size/volume calculation: standard ellipsoid equation ( L × W × H ) using
varying correction factors – depending on bladder shape (0.5 for spherical/ellipsoid confi guration, 1.0 for rectangular shape). See above.
• Normal bladder volume varies with age; simplifi ed estimation of age-related
bladder volume = [age (in years) +2] × 30 (ml).
Always pre-/post-void volume should be compared, difference calculated to assess
pathologic residual volume (>10 %/>20 ml).
• Physiologically residual urine noted in neonates (immature bladder function)
and after nonphysiological voiding situations.
Ureteric infl ow may be seen on gray scale:
• CDS will improve depiction of ureteric jet, which usually should be symmetric
and regular – helps depiction of asymmetric ostium position or asymmetric urine
infl ow (see Fig. 10.1 ).
NOTE : All respective sections have to be documented.
10.7.2 Pathologic Findings
10.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
Nonphysiologic tension even with little fi lling, volume, signs of dysfunction (open
bladder neck), thickened trigone, thickened bladder wall, reduced/enlarged capacity, trabeculation, pseudo-diverticula; atypical position/number/shape of ostium
(e.g. gapping ostium), etc. (Fig. 10.39 ):

372
abc
Fig. 10.40 Bladder polyps . ( a , b ) Typical polyps of bladder wall (+ +) with typical vascular
pedicle depictable by aCDS ( a ) or CDS ( b ). Bl bladder. ( c ) Polypoid structure (+ +) reaching into
bladder through bladder neck, in a child with a fi broid polyp of the posterior urethra
10 Ultrasound of the Urogenital Tract
ab
Fig. 10.41 Bladder wall (pseudo)tumours and DDx. ( a ) Bladder rhabdomyosarcoma: caulifl ower-
like polypoid tumour growing into bladder lumen, with broad attachment to bladder wall. ( b )
Regional thickening of bladder wall in a child with neurofi bromatosis Type I, consistent with
bladder wall neurofi broma (+ +)
• (Secondary?) Dilatation of distal ureter with stenosis by thickened bladder wall,
ureteral junction stenosis (obstructive megaureter – UVJ obstruction, see below),
dysplastic/immotile segments, obstructing concretions
10.7.2.2 Polyps
Arising from the wall or entering through bladder neck (urethral fi broepithelial
polyps).
May exhibit central vessel arising from bladder wall (Fig. 10.40 ).
10.7.2.3 Bladder Tumours
Rare in children.
Either diffusely infi ltrating wall with wall thickening (e.g. neurofi broma), arising
from wall/growing into lumen or into paravesical space in caulifl ower-like appearance (mostly rhabdomyosarcoma) or also arise from adjacent structures infi ltrating
bladder (e.g. from prostate/vagina).
US nonspecifi c, may exhibit vascularity (Fig. 10.41 ).
DDx: clots/fi brin (may be adherent to wall, then positioning manoeuvres do not
help for differentiation, as they then do not change position), pseudotumours in
atypical or haemorrhagic infection, polyps.

10.7 US of Urinary Bladder
Fig. 10.42 Bladder wall calcifi cation. Echogenic inner layer of thickened bladder wall in
amoebiasis
10.7.2.4 Calcification in/of Bladder
Typically in advanced schistosomiasis – with an echogenic layer in thickened bladder wall, usually with reduced bladder capacity/increased bladder tension
(Fig. 10.42 ). Also urolithiasis may occur in bladder after passing from above or
(infectious) stones grow in bladder (e.g., after / during infection, in cystinuria...)
DDx: thickening of bladder endothelium in infl ammation (cystitis) with free-
fl oating particles in lumen, bladder sedimentation (blood, proteins, cells, concentrated
urine, crystals, concretions – particularly large stones in oxaluria/cystinuria, etc.).
373
10.7.2.5 Ureterocele
Cystiform end of ureter protruding into bladder lumen at ostium:
• Orthotopic ureterocele usually draining single renal system, central opening.
• If associated with duplex kidney then typically positioned at more distal-medial
position entering ureter that drains upper moiety of duplex system, often causing
megaureter. Usually have opening at mediocaudal aspect of ureterocele.
US / CDS Findings
• Cystic structure protruding into bladder of varying size.
• Large ureteroceles may herniate into bladder neck causing obstruction during
voiding (Fig. 10.43 ).
• May also drain ectopically, protrude into vagina or paravesically/proximal ureter,
seminal vesicles, etc.
• Urine infl ow jet depictable by CDS – helps differentiating ectopic versus orthotopic ureterocele and assessing degree of obstruction/patency.
NOTE : (Small) Ureteroceles may collapse with poor diuresis – suffi cient bladder
fi lling, observation over some time during peristaltic wave, and suffi cient hydration
essential not to miss small ureteroceles. May also evert forming a adiverticulum
with increased intravesical pressure (e.g. full bladder, during voiding) – then
respective ureter may become refl uxing.
10.7.2.6 Persisting Urachus
Fetal remnant, physiologically seen in fi rst weeks of life, usually regresses.
Considered pathologic if with central lumen that drains bladder to umbilicus, or
persisting into infancy/childhood.

374
10 Ultrasound of the Urogenital Tract
a
d
Fig. 10.43 Ureterocele. ( a ) Typical image of a ureterocele protruding into bladder lumen like a
cyst at site of the ostium. ( b ) Parasagittal oblique section through ureterocele depicts correspond-
ing megaureter (+ +) behind bladder. ( c ) Small collapsed ureterocele in an insuffi ciently hydrated
child – only some ostial irregularity and thick wall of ureterocele (+ +) depictable by meticulous
scanning. ( d ) Ectopic ureterocele (
thra. ( e , f ) ce-VUS in a duplex kidney with ureterocele: observe non-contrasted ureterocele ( UC )
with respective megaureter ( MU ) ( e ), contrast refl ux into the other dilated ureter ( U ) up to grossly
dilated lower moiety ( f , oblique section)
b
e
+ …+) behind bladder, potentially draining into vagina or ure-
1
c
f
a
Fig. 10.44 Urachus. ( a , b ) Typical appearance of band-like structure (+ +) connecting bladder roof
to umbilicus. Close-up ( a ) and overview ( b ); no lumen visualised – however this may be missed
with poor bladder fi lling. ( c ) Axial section through full bladder: tumour-like nodule in bladder wall
on bladder roof, consistent with a physiological urachal remnant – not to be mistaken for tumour
b
c
US Findings
String-like structure seen even with poor bladder fi lling using high-resolution linear
transducers, coursing in midline close to abdominal wall, from bladder roof to
umbilicus (Fig. 10.44 ).
For assessment of patency and lumen, good bladder fi lling essential:
• Potentially need to fi ll bladder with saline and/or US-CM (as done for fl uoroscopy), or also by careful injection of umbilical opening.
Remnants of urachus may persist in form of urachal cyst/diverticula – may get
infected, seen as complex cystic/abscess-like structure along course of urachus.

10.7 US of Urinary Bladder
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NOTE : Physiological remnant of urachus may cause pseudotumourous nodule in
bladder wall at bladder roof – physiologic, should not be mistaken for bladder
tumour.
10.7.2.7 Megaureter
Dilatation of distal ureter, varying dilatation in middle/proximal portion.
Can be obstructive (stenotic uretero-vesical junction – uretero-vesical junction
obstruction – UVJO), refl uxive (high-grade dilating refl ux with gapping ostium and
changing size) or dysplastic (primary megaureter) with dysplastic segment that has
less muscle and no peristalsis.
US Findings
Dilated ureter, with/without peristalsis; often with some thickening of urothe-
lium/ureteral wall.
Try to always fi nd ostium (often associated with slightly altered position, com-
monly more medially and distally in obstructive types, more lateralised and cranially in refl uxive types).
Always assess tortuosity, peristalsis (documentation with M-Mode/cine-loop
clips helpful) as well as varying dilatation of renal collecting system. May be associated with duplex kidneys (see Figs. 10.7 and 10.15 ).
NOTE : For depicting and evaluating megaureters (initially and follow-up), standardised hydration/suffi ciently fi lled bladder mandatory.
10.7.2.8 Infravesical Obstruction
Most commonly posterior urethral valve (PUV, nearly always in baby boys).
Other forms of infravesical obstructions may be strictures and stenosis
(rare), partial valves/folds, concretions, tumours (arising from prostate or pelvic floor), urethral malformations (diverticula, duplex urethra, severe hypospadias, etc.).
Rarely fi stulae may exist – diffi cult to visualise on US.
US Findings
Suspected by indirect signs (bladder wall thickening, open bladder neck, trabeculation, megaureters, etc.).
Directly visualised on perineal/penile US with open bladder neck, particularly
during/attempts of voiding – shows typical dilatation of posterior urethra in PUV
(or tumour/site of compression) (see Figs. 10.6 and 10.19 ).
NOTE : ce-VUS/perineal US can usually depict PUVs when assessed during
voiding.
Additional Investigations
VCUG/urethrography, cystourethroscopy.
For tumours/in future MR urethrography.
10.7.2.9 Inflammation
Isolated cystitis or part of UTI involving also upper tract(s).
US / CDS Findings
More or less thickened bladder wall, particular inner mucosal layer.

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Echoes within lumen:
• Potentially widening and laxity of ureters, with urothelial sign (wall thickening).
• Hypervascularity of bladder wall, fl ash echoes within lumen, pronounced urine infl ow
jet from affected kidney; on spectral analysis diastolic hyperemia of these vessels.
NOTE : Diagnosis, however, always made by urine analysis. Isolated cystitis not
considered a mandatory indication for VUR testing any longer.
10 Ultrasound of the Urogenital Tract
10.7.2.10 Traumatic Changes
Intravesical clots, haematoma of bladder wall, bladder rupture. The latter (particularly in conjunction with inconsistent history) suspicious for NAI.
US Findings
• Clots : more or less spherical formations of intermediate and potentially inhomo-
geneous echogenicity in bladder lumen; may be adjacent/fi xed to wall by fi brin
layers. Can become large and cause (intermittent) obstruction.
• Wall haematoma appears as tumour-like thickening with changing echogenicity –
depending on age of haematoma.
• Rupture : site of rupture sometimes diffi cult to see, only after fi lling via catheter.
Most common observation – reduced bladder capacity and perivesical fl uid
(intra- or extraperitoneal).
10.7.2.11 Vesico-ureteric Reflux
See respective entry above.
10.7.3 Paravesical Changes
Suffi ciently fi lled bladder – ideal window to deeper pelvic spaces, for assessment of
internal genitalia, rectum/bowel, pouch of Douglas.
Typical US Findings
Free fl uid, may be simple (no echoes – simple ascites) or complex (with echoes, sedimentation, fi brin bands – e.g. after trauma/haemorrhage, in peritonitis/infl ammation).
TIP : Digital rectal palpation during real-time US may improve potential to defi ne
origin/entity. Potentially fi ll bladder/rectum by saline infusion.
10.7.3.1 Abscess Formations
Typical complication of perforated appendicitis, other bowel infl ammatory conditions with perforation, adnexal infl ammation; may also arise from urachus remnants –
see respective chapters.
US commonly shows formation with typical wall, with hypervascularity on
CDS, centrally fi lled of complex fl uid, potentially with sedimentation and some
included air; sometimes coproliths may be found with in abscess (see Fig. 9.24 ).
10.7.3.2 Tumours of Paravesical Region
Most commonly arise from pelvic fl oor, internal genitalia (rhabdomyosarcoma,
ovarian tumours), sacrum (most commonly sacral teratoma) and neuroblastoma/
ganglioneuroblastoma or PNET (which may arise presacrally).
No specifi c US signs – see respective chapters.
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