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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

10.3 Pathology of the Kidney
a
bc
de
Fig. 10.30 Urinary tract trauma. ( a ) Blood sedimentation in urinary bladder after renal trauma.
( b ) Perirenal clear fl uid – consistent with posttraumatic urinoma. ( c , d ) Focal altered contour and
structure of kidney ( c ) after trauma – only aCDS ( d ) clearly demarks extent of renal injury. ( e )
Relatively normal appearance of kidney, but no perfusion on aCDS (colour box) – indicating
devascularisation due to hilar injury of the kidney
357
10.3.9 Renal Tumours
10.3.9.1 Benign Tumours
Mostly hamartoma, angioma, angiomyolipoma (tuberous sclerosis) and rarely
adenoma.
10.3.9.2 Pre- or Semimalignant Tumours
Nephroblastomatosis (remnants of metanephrogenic tissue, may develop into Wilms’
tumour), neonatal mesoblastic nephroma (mostly benign, rare malignant entities).
10.3.9.3 Malignant Tumours
Most commonly Wilms’ tumour (nephroblastoma), rhabdoid tumour, renal sarcoma, renal cell carcinoma – other entities rare.
US Findings (Fig.
10.31 ):
• Angiomyolipoma exhibits more or less typical echogenic tissue structure.
• Cystic nephroma appears as multicystic mass that may manifest segmentally
with tumourous enlargement, disruption of normal echogenicity, small septae,
usually with little perfusion. Larger solid areas, nodular wall structure, hyperaemia or large cystic components with haemorrhage may indicate another underlying entity (e.g. cystic Wilms’ tumour).

358
a
bc
10 Ultrasound of the Urogenital Tract
d
g
ef
h
ijk
Fig. 10.31 Renal tumours. ( a ) Focal echogenic renal tumour, typical for an angiomyolipoma. ( b , c )
Focal renal tumour of similar echogenicity as renal cortex on gray scale ( b ), better visible by its exophytic
behaviour and its (hyper)vascularity on CDS ( c ), in a patient with tuberous sclerosis – consistent with an
atypical angiomyolipoma – needs follow-up and sectional imaging. ( d ) Nephroblastomatosis: multiple
peripheral renal tumourous nodules, partially diffi cult to appreciate on gray scale, better outlined by aCDS.
( e ) Typical appearance of Wilms tumour: large mass with relatively homogenous tissue and cortex-like
echogenicity. ( f , g ) More and less cystic Wilms tumours. ( h ) 3DUS in an echogenic Wilms tumour, helpful
for more accurate tumour volume calculation; the right lower box shows a 2DUS image of same patient
with an additional exophytic nephroblastomatotic focus in upper pole (
system caused by impaired drainage due to compression of renal pelvis by the large tumour. ( i ) Focal renal
+…+) in a child with lymphatic leukaemia – consistent with renal involvement. ( j ) (Congenital)
lesion (
1
Renal tumour in a neonate with subtotal destruction of kidney, only leaving a subtle peripheral rim of original kidney parenchyma – consistent with a mesoblastic nephroma. ( k ) Atypical tumour (
girl. Most common DDx: rhabdoid Wilms tumour, renal sarcoma, renal cell carcinoma
+…+). Note dilatation of collecting
1
+…+) in an older
1

10.4 Renal Biopsy and Interventions
359
• Other tumours have nonspecifi c appearance of any mass lesion – may exhibit
pseudocapsule, growth from kidney, displacing surrounding structures, local
lymph node metastases and – particularly in Wilms’ tumour – relatively often
have vascular invasion with renal vein thrombosis reaching even into IVC and
up to right atrium (may also occur in renal cell carcinoma). Secondary necrotic,
cystic, haemorrhagic changes may be present.
• Assumption of entity depends more on age than on US/imaging fi ndings.
• Tumours usually large when diagnosed (different for angiomyolipoma/hamartoma).
DDx
Focal nephroma/infl ammatory pseudotumour, xanthogranulomatous pyelonephritis, infi ltration in systemic disease (lymphoma), hypertrophic column of Bertin,
other complex cysts.
Role of US
Initial diagnosis – fi nd/confi rm suspected lesion, defi ne size (volume calculation)/
relation to central renal structures, surrounding organs/tissue, assess patency of central structures (artery, vein, pelvis), give fi rst information on stage (infi ltrating/local/
liver metastases?).
Later-follow-up, assessment of complications.
Additional Investigation
• Sectional imaging by MR (or CT, if MR unavailable) mandatory, particularly in
suspected malignancy – adhere to local tumour imaging protocols.
• Sometimes US-guided biopsy (varies with country/continent).
10.4 Renal Biopsy and Interventions
Also see Chap. 2 for general recommendations/guidelines.
10.4.1 Renal Biopsy
Biopsy often necessary for histologic assessment of renal parenchymal disease –
biopsy of focal renal lesions far less common than in adults, particularly in Europe.
Renal biopsy should always be performed under US guidance for reducing risks:
• Standardised procedure with pre-interventional assessment, time out, periinterventional guidance, postinterventional follow-up.
• Standardised protocols should be used.
• Pre-interventional US performed to assess kidney for potential dilatation, thickness of renal parenchyma, potential biopsy risks (e.g. abnormal vessels or preexisting arteriovenous malformations/fi stula) and impaired access. At that time
needle length/size defi ned – depending on depth of kidney, size of sample
required, thickness of parenchyma.
• Most commonly 20–18(−16) Gauge needles with 1.2(−2) cm core length advisable, potentially using coaxial technique.
• Use of steering device (biopsy guide) and (semi-)automated biopsy guns helpful.
• Thereafter validation of indication and coagulation check, informed consent,
time out.

360
ab
10 Ultrasound of the Urogenital Tract
c
de
Fig. 10.32 Renal biopsy. ( a ) Renal biopsy, dorsal approach to lower pole of left kidney: needle path
outlined by dotted lines , needle (echogenic line) already advanced to renal capsule. ( b ) Needle now
fi red, position and depth of needle nicely visualised by image from cine-loop documentation. ( c )
aCDS superiorly helps to depict postinterventional subcapsular haematoma which in early stages is
of similar echogenicity as renal cortex; also observe triangular perfusion defect in lower pole, indicating regional perfusion defect due to injury of respective vessel causing a small infarction. ( d , e )
Postinterventional follow-up (3 h after procedure) depicts focal aliasing on CDS, consistent with an
arteriovenous fi stula; respective fl ow alterations of feeding artery and draining vein assessed by
spectral analysis (e) confi rming shunt fl ow by demonstrating arterialised fl ow pattern in draining vein
• US - guided biopsy (see also Chap. 2, and Figs. 2.12 and 2.13 ): performed in
prone position (for native kidneys) – with support under belly to avoid displacement of lower pole of left kidney (usually targeted to avoid injury of adjacent
liver on right side).
– Local and systemic analgesia/sedation may be necessary with adequate
monitoring.
– Biopsy direction – parallel to major segmental vessels branching into periph-
ery; CDS helpful to avoid large vessels.
– Real-time monitoring of needle positioning and biopsy using cine loop
advisable.
• Post-biopsy US: check for potential post-biopsy complications (e.g. bleeding,
haematoma, haematuria, infarction and AV fi stula), recommended immediately
afterwards, 3–6 h and 24 h after intervention. Standardised post-biopsy management helpful (Fig.
10.32 ).
• See also ESPR/ESUR recommendations in Pediatr Radiol (2014 -in press).
10.4.2 Drainage/Nephrostomy
US enables safe access to dilated system or abscess. Steering devices attached to
transducer sometimes helpful; alternatively freehand technique used. Always defi ne

10.4 Renal Biopsy and Interventions
361
adequate access that allows for suffi cient parenchymal coverage of targeted area to
avoid leakage/urinoma formation.
Access achieved commonly using trocar or Seldinger technique; additional sup-
plementing fl uoroscopy may be helpful to assess leakage, positioning and anatomy
after contrast instillation once successful access is gained under US guidance or for
Seldinger technique using guide wires and dilatation of parenchymal tract (see
Chap. 2 , and Figs. 2.14 and 1.13 ).
10.4.3 Postoperative Imaging
To assess postoperative anatomy, to detect complications and to evaluate success.
For assessment of VUR recurrence or insuffi cient success of cystoscopic tech-
niques, ce-VUS can be performed as alternative to VCUG even intraoperatively.
10.4.3.1 After VUR Treatment
Cystoscopic Treatment
Injection of material at ostium under cystoscopic guidance
US can assure patency of ostium by proving ureteric infl ow jet, may depict
impaired drainage (too large deposits), causing ureteral/pelvi-caliceal distension,
potentially associated with stenotic peristalsis of ureter.
Deposits usually seen as echogenic focus in vicinity to transmural distal ureter
– may cause twinkling (Fig. 10.32 ).
NOTE : Some transient dilatation of ureter normal, may disappear
spontaneously; only if additional new dilatation of pelvi-caliceal system noted,
obstruction needs to be considered – then may need further functional
assessment/potentially guided drainage/stenting.
Antireflux Surgery
Different surgical techniques used, ostium appearance varies depending on performed surgery:
• Commonly altered course/potentially altered insertion of ureter visualised.
• Ureter infl ow jet more diffi cult to depict.
• Initially ureteric wall thickened/swollen, some ureteral dilatation.
• Only in signifi cant obstruction higher degree of dilatation of collecting system
observed – some transient mild dilatation often seen in early postoperative phase, particularly if drains acting as foreign body placed causing reduced ureteral peristalsis.
NOTE : With full bladder there may be kinking of ureter at insertion causing (tran-
sient? intermittent?) obstruction.
Other complications:
• Rarely perivesical haematoma/urinoma – will usually resolve spontaneously
provided suffi cient bladder drainage.
• Rarely intervesical clots, commonly catheters (often placed for fi rst days).
NOTE : Search for bladder wall injury with urinoma formation, try to localise
potential drains.
Findings in reimplantation for megaureter similar as with antirefl ux surgery
– preexisting dilatation of ureter and wall thickening persist, even in good result
with good function.

362
a
bc
10 Ultrasound of the Urogenital Tract
de
Fig. 10.33 Postoperative US. ( a ) Swollen ostium after reimplantation of a megaureter; patency docu-
mented by CDS exhibiting ureteric infl ow jet. ( b ) Echogenic deposit at ostium after cystoscopic treat-
ment of VUR (defl ux instillation). ( c ) JJ catheter in physiologically stilldilated renal pelvis after
pyeloplasty. ( d ) Dilated renal collecting system after surgery, with sedimented echoes in calyx, consis-
tent with postoperative intraluminal blood. ( e ) Perivesical fl uid accumulation after accidental injury to
bladder wall in cystoscopic unroofi ng of a huge ureterocele, consistent with a perivesical urinoma
10.4.3.2 Findings After Pyeloplasty
Early assessment should focus on depiction of perfusion defi cits – persisting dilatation normal, does not indicate persisting obstruction:
• Assess position of drain/tip of JJ stent, potentially urinoma/haematoma and postoperative infarctions. Furthermore haematoma/echoes in collecting system (Fig. 10.33 ).
• Asymmetrically elevated RI/slightly impaired renal perfusion physiologic in
early postoperative setting. Sometimes sectional infarction (vascular damage).
• Perfusion should normalise unless persisting obstruction/chronic damage/scarring is present.
• In early state dilatation often less due to stents or drains – when withdrawn,
some (particularly intrarenal) dilatation persists, degree of extrarenal dilatation
depends on amount of resected pelvis, does not correlate with potentially
persisting obstruction. Only gradually dilated system will eventually become
narrower over time, renal pelvis usually is immediately smaller due to partial
resection perioperatively – does not indicate absence of obstruction.
• Physiologically some transient increased echogenicity with reduced corticomedullary differentiation (reactive swelling).
• Eventually renal parenchyma normalises – except for those with scarring/persistent damage.
• Renal (parenchymal) growth best monitored using volume calculations – also try
to assess pelvi-ureteric junction, ureteric infl ow jet into bladder, potentially additional vessels and scarring.
• Additional imaging: MAG3 scintigraphy and/or MR urography, rarely focused IVU.

10.5 Re na l Transplant
NOTE : US poor in assessing/grading drainage – achieved by scintigraphy/MR
urography; some centres perform pressure tests before withdrawal of postoperative
catheter from collecting system under fl uoroscopic surveillance (pressure point for
contrast drainage into ureter should be <10 cm H 2 O).
363
10.4.3.3 After Various Interventions
A variety of interventional procedures exist – balloon dilatation, percutaneous
drainage/stenting, endoscopic unroofi ng of ureteroceles, etc.
After Biopsy , Drainage , etc. – See above.
US Findings after other interventions :
Depend on performed procedure. Used to evaluate/document dilatation of collecting system, potential echoes/structures within system, position of drainages and
stents, assessment of haemorrhage or urinoma and renal perfusion.
After Extracorporeal Lithotripsy ( ESWL )
• Assess residual concretions, amount of disintegration and potential persisting
obstruction (particularly at site of ureteropelvic/uretero-vesical junction) by
residual deposits.
• Tissue damage by shock wave (oedema, haematoma/diffuse swelling/rupture –
either of surrounding tissue and/or kidney).
• Some transient perfusion impairment (reduced peripheral vasculature on aCDS,
elevated RI due to low diastolic fl ow) – commonly resolves spontaneously.
10.5 Renal Transplant
US used for pre-, peri-, post-transplant assessment (see also ESPR/ESUR recommendations in Pediatr Radiol 2014, in press):
• Pre-transplant assessment of donor: assess potential preexisting conditions;
insure that living donor left with suffi ciently functional kidney.
• Recipient evaluation: preexisting renal disease, bladder (capacity/function), major
vessels for planning anastomosis (diameter, patency, course of arteries and veins).
• During transplantation: CDS to assess perfusion of freshly implanted kidney
(to depict early potential compromise of vascular anastomosis allowing for
immediate repair).
• After transplantation: repeated follow-up to assess for proper function/potential
complications.
10.5.1 Normal US Findings in Renal Transplant
Commonly large, in right/left iliac fossa, size/shape depend on donor organ. Corticomedullary differentiation often pronounced. CDS exhibits normal vascular architecture
– some transient aliasing at anastomosis during early postoperative period; use aCDS to
demonstrate peripheral normal (perfused) vasculature. Segmental perfusion defects may
correspond to site of biopsy/infarctions (e.g. sacrifi ced accessory/polar arteries). Spectral
trace of arterial and venous fl ow profi les as in normal healthy kidneys (Fig. 10.34 ).

364
a
bc
10 Ultrasound of the Urogenital Tract
def
Fig. 10.34 Renal transplant/PTLD. ( a ) Typical appearance of the parenchyma of a renal trans-
plant, with prominent cortico-medullary differentiation; pelvis visible, also some fl uid at upper
pole. ( b ) aCDS demonstrates normal peripheral vascularity; reduced colour coding of medullae is
physiological. ( c ) CDS with spectral trace shows altered and reduced arterial peripheral fl ow and
markedly turbulent and accelerated venous fl ow due to severe renal swelling– a sensitive, but nonspecifi c sign (in this case rejection). ( d ) Perirenal fl uid collection – DDx: postoperative urinoma,
liquefi ed haematoma, lymphatic fl uid collection. ( e ) Focal complex hypoechoic liquid lesion adja-
cent to vascular anastomosis with preserved fl ow in vessels – seromatous transformation of a
perivascular postoperative haematoma (DDx: thrombosed aneurysm). ( e ) Focal hypoechoic nodule
in transplanted kidney; the child also had similar nodules in original kidney as well as a group of
enlarged mesenteric nodes, consistent with PTLD
NOTE : RI changes nonspecifi c – depend on number of partially systemic/extrare-
nal factors. Persisting singularly renal fi ndings such as elevated RI (> 80), increased/
fast venous fl ow, pathologic fl ow pattern (e.g. delayed systolic upstroke, aliasing/
turbulence), etc. Indicate transplant problems, as well as signifi cantly decreased
(peripheral) perfusion, particularly on aCDS (e.g. peripheral halo/rim sign).
10.5.2 Pathologic US Findings
Early Post - transplant Findings (Fig. 10.34 ):
• Perirenal haematoma, cyst formation – may represent lymphocele, urinoma.
• More or less dilatation of collecting system with potentially swelling/thickening of
urothelium.
• Peripheral zones of contusion or infarction (e.g. site of initial biopsy).
• Malposition of drain/catheter – fi ndings comparable to respective US appearance
in native kidney.
• aCDS: assess focal turbulent fl ow, peripheral minor perfusion, segmental perfusion defects – guide spectral analysis.
• Spectral analysis: impaired diastolic fl ow, impaired systolic infl ow, missing/
turbulent venous fl ow – signs for vascular complications.

10.6 Adrenal Glands and Pararenal Space
NOTE : US poor in differentiating between various causes of acute transplant failure
(e.g. acute tubular necrosis, acute ischaemia, renal vein thrombosis, acute rejection).
• DDx narrowed by clinical signs with detailed history of surgery, US features –
eventually may need US-guided biopsy.
Late Post - transplant Findings
Entities : Lymphocele, infection, cyclosporine toxicity, vasculopathy/stenosis/aneurysm, rejection, urinary obstruction. Most fi ndings refl ect respective sonomorphologic features in native kidney.
Rejection :
Most sensitive sign – acute enlargement of transplant organ, RI not specifi c (tend to
be elevated). In suspected rejection only renal biopsy will eventually establish or
exclude the diagnosis:
• Some centres perform protocol driven biopsies; others only perform biopsy on
clinical indication.
NOTE : Helpful to have baseline US in stable uneventful post-transplant period to
allow for comparison during phases with transplant complications. Always include
assessment of potentially remaining native kidneys (e.g. cystic disease,
tumour) + major abdominal structures (e.g. post-transplant lymphoproliferative disease – PTLD, Fig. 10.34 ) on follow-up US.
Role of US
• Major imaging tool for assessment and follow-up, also at bedside.
• May help decisions on additional imaging.
Additional Investigations
• VCUG/ce-VUS, scintigraphy, MR urography/angiography.
• Rarely CT, interventional radiology for potential percutaneous treatment.
365
10.6 Adrenal Glands and Pararenal Space
10.6.1 General Remarks
Prominent in fi rst months of life (length 10–12 mm), will then shrink to approximately 50 %.
Thereafter constant growth over years – eventually ends in puberty with normal
size (length ~ 2 cm). Medulla prominent in neonate; cortex later becomes prominent.
10.6.2 Typical Normal US Finding
V- or Y-shape structure situated on upper pole of kidney (Fig. 10.35 ):
• Shape variable, particularly in ectopic position of kidney.
• Centrally echoic, less echoic peripheral cortex, surrounded by more or less echogenic perirenal fat.
NOTE : In neonates adrenal gland easy to visualise; the older and more obese a
patient, the more diffi cult to assess by US.
Volume :
Various methods with partially complicated calculations reported. Rough estimate
of size achieved by maximal sagittal length.

366
ab c
Fig. 10.35 Normal adrenal gland. ( a ) Normal shape and appearance of adrenal gland in neonate.
( b ) Enlarged view nicely showing typical neonatal differentiation of adrenal medulla and cortex.
( c ) Atypical shape of neonatal adrenal gland due to missing right kidney
10 Ultrasound of the Urogenital Tract
NOTE : Differentiation of prominent adrenal gland (e.g. reactive to stress/other
physiologic conditions) from hyperplasia/enlargement in other conditions may be
impossible.
Normal variations :
Hypoplasia/aplasia; associated with severe hormonal defi cits if bilateral.
Hypertrophy/hyperplasia diffi cult to defi ne sonographically, usually in combination
with clinical symptoms/syndrome and respective hormonal fi ndings.
10.6.3 Pathologic Findings
10.6.3.1 Adrenal Gland Haemorrhage
Typically in newborns, asphyxia, after trauma/stress – but also with sepsis, systemic
conditions.
• May occur fetally. Varies in size, uni- or bilateral.
• May cause displacement of surrounding structures (e.g. thus impairing renal
blood fl ow with consequent renal vein thrombosis).
• Rupture/retroperitoneal haematoma/haematoperitoneum extremely rare.
US Findings
• Initially inhomogeneously echogenic enlargement of adrenal gland with shape of
complex cyst (Fig. 10.36 ).
• Then increasingly hypoechoic with complex liquid aspect, septations,
sedimentations.
• Shrinkage/resolution, potentially with some remnant calcifi cation (echogenic,
with dorsal shadowing):
• Usually easy to differentiate from similar entities.
CDS : haemorrhagic cyst, complex dysplastic upper moiety of duplex kidney, para-
renal/subcapsular haematoma, psoas haematoma/abscess, urinoma, cystichaemorrhagic tumour.
Role of US :
In neonates US the ideal method; in older children sectional imaging may become
necessary, as well as in equivocal situations (provided a therapeutic consequence).
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