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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Preface for the Second Edition
- •Acknowledgements
- •Contents
- •1: US Physics
- •1.1 US Waves
- •1.2.5 Deflection
- •1.2.6 Focus
- •1.2.7 Resolution
- •1.3.1 Emission
- •1.3.2 Transmission
- •1.3.3 Reception
- •1.3.4 Amplification
- •1.4 Signal Processing
- •1.4.1 Preprocessing
- •1.4.2 Post-Processing
- •1.4.3 Time Gain Compensation (TGC)
- •1.4.5 Gain
- •1.4.6 Frame Rate/Persistence
- •1.5.1 Transducers
- •1.6 Modern US Techniques
- •1.6.1 High-Resolution US (HR-US)
- •1.6.2 Image Compounding
- •1.2.1 Acoustic Impedance
- •1.2.2 Impedance Change
- •1.2.3 Reflection
- •1.2.4 Absorption
- •1.6.3 Harmonic Imaging (HI)
- •1.6.5 US Texture Analysis
- •2: US Methods, Artefacts, Biologic Effects, Practice
- •2.1 A (Amplitude)-Mode
- •2.2 (T)M-Mode (Time-Motion-Mode)
- •2.3 B (Brightness)-Mode
- •2.4 Doppler Sonography
- •2.5 Artefacts
- •2.5.1 General Remarks
- •2.5.2 Common Artefacts
- •2.5.2.1 Side Loop Artefact
- •2.5.2.2 Bowing Artefact
- •2.5.2.3 Noise
- •2.5.2.4 Marginal Shadowing
- •2.5.2.5 Posterior Enhancement—Increased through Transmission
- •2.5.2.6 Reverberation Artefact
- •2.5.2.7 Increment or Slice Thickness/Beam Width Artefact
- •2.5.2.8 Mirror Image Artefact
- •2.5.2.9 Shadowing
- •2.5.2.10 Refraction Artefact
- •2.5.2.11 Anisotropy
- •2.6 Biologic Effects
- •2.6.1 General Remarks
- •2.6.2 Thermal Effects
- •2.6.2.1 Tissue Heating
- •2.6.2.2 Biological Effects, Tissue Heating
- •2.6.3.1 Cavitation
- •2.6.4.1 Specific Risks
- •2.6.5.1 Mechanical Index (MI)
- •2.6.5.2 Thermal Index (TI)
- •2.7.1 Requisites
- •2.7.1.1 Indications
- •2.7.1.2 Environmental Requisites
- •2.7.2 Positioning
- •2.7.3 Device Handling
- •2.7.3.1 General Remarks
- •2.7.4 Transducer Selection
- •2.7.4.1 General Remarks
- •2.7.4.2 Neurosonography (See Chap. 8)
- •2.7.4.4 Chest US (See Chap. 12)
- •2.7.4.5 Abdominal US (See Respective Chapters)
- •2.7.5.1 General Remarks
- •2.7.5.2 Transducer Handling
- •2.7.5.3 Measurements
- •2.8.1 Image Documentation
- •2.8.2 Report
- •2.8.2.2 Diagnosis
- •2.8.2.3 Predefined Reports
- •2.8.2.4 Nomenclature
- •3.1 Doppler Sonography
- •3.1.1 The Doppler Phenomenon
- •3.1.2.1 Continuous Wave Doppler (CW)
- •3.1.2.2 Pulsed Wave Doppler (PW)
- •3.1.2.3 Duplex-Doppler Sonography/Spectral Flow Analysis
- •3.1.2.5 Amplitude-Coded Colour Doppler Sonography (aCDS)
- •3.1.2.6 Other Flow-Sensitive US Techniques
- •3.2.1 Aliasing
- •3.2.2 Spectral Broadening
- •3.2.3 Sample Volume Artefact
- •3.2.4 Filtering Artefacts
- •3.2.5 Scaling Problems
- •3.2.6 Gain-Induced Errors
- •3.2.7 Angle Correction
- •3.2.8 Motion Artefact
- •3.2.9 Twinkling Artefact
- •3.2.10 Others
- •3.3.1 Limitations
- •3.3.2 Interpretation
- •3.4.2 Typical Paediatric 3DUS Applications
- •3.4.2.1 Neonatal Neurosonography
- •3.4.2.7 Other Potential 3D-/4DUS Applications
- •3.4.5 Potential Future Paediatric 3DUS Applications
- •4.1 Contrast-Enhanced Ultrasound (ce-US)
- •4.1.1 Basics
- •4.1.2 ce-US Applications-General Remarks
- •4.1.3 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •3.4.2.3 Urinary Bladder 3DUS
- •3.4.2.5 Musculoskeletal 3DUS Applications
- •3.4.2.6 Small Part 3DUS Applications
- •4.1.5 Intravenous ce-US (CEUS)
- •4.1.5.2 Dose Recommendations
- •4.1.6 Future ce-US Potential
- •4.2 Ultrasound-/Sonoelastography
- •4.2.1 Methods
- •4.2.1.1 Strain Elastography
- •4.2.1.2 Transient Elastography (TE)
- •4.2.1.3 Shear Wave Elastography (SWE)
- •4.2.2 Applications
- •4.2.2.1 Focal Lesions
- •4.2.2.2 Diffuse Changes
- •4.2.2.3 Possible Indications—Summary
- •5.1 Requirements
- •5.2 Typical Applications
- •6.1 Introduction
- •6.2.1 Urinary Tract Infection (UTI)
- •6.2.3.1 Pelvi-Ureteric Junction Obstruction (PUJO)
- •6.2.3.3 Gross Vesico-Ureteric Reflux (VUR)
- •6.2.4 Urolithiasis (and Nephrocalcinosis)
- •6.2.5 Cystic Kidney Disease (CKD)
- •6.2.6 Torsion (Ovary, Testis)
- •6.2.7 Genital Malformations
- •6.2.8 Renal Hypertension
- •6.3.1 Necrotizing Enterocolitis (NEC)
- •6.3.3 Acute Abdomen
- •6.3.4 Acute Appendicitis
- •6.3.5 Splenomegaly
- •6.3.6 Cholestasis
- •6.3.7 Pancreatitis
- •6.3.8 Biliary Atresia
- •6.3.9 Abdominal Trauma
- •6.3.10 Abdominal Tumours
- •6.4.1 Pneumonia, Pleural Effusion
- •6.4.2 Enlarged Mediastinum
- •6.4.3 Painful Hip/Limping Child: Osteomyelitis
- •7.1 General Considerations
- •7.3.1 Miscellaneous Other Considerations
- •8.1 Requisites
- •8.2 Normal Findings
- •8.2.1 Transfontanellar Access
- •8.2.2 Alternate Access Findings
- •8.2.3 Colour Doppler Sonography (CDS)
- •8.2.4.1 Periventricular Echogenicities
- •8.2.4.2 Ventricular Asymmetry
- •8.2.4.3 Ventriculomegaly
- •8.2.4.4 Cisterna Magna
- •8.2.4.5 Vascular Variations
- •8.3 Pathologic Findings
- •8.3.1 Neural Tube Defects
- •8.3.1.1 Anencephaly
- •8.3.1.3 Arnold Chiari Malformation
- •8.3.1.4 Dandy–Walker Malformations/Spectrum
- •8.3.1.5 Corpus Callosum Malformations
- •8.3.1.6 Lipoma
- •8.3.2.2 Megalencephaly
- •8.3.2.3 Schizencephaly
- •8.3.2.4 Holoprosencephaly
- •Alobar Holoprosencephaly
- •Semilobar Holoprosencephaly
- •Lobar Holoprosencephaly
- •De Morsier Syndrome: Septo-Optic Dysplasia
- •8.3.2.5 Hydranencephaly
- •8.3.3 Phakomatoses
- •8.3.4 Cerebral Cysts
- •8.3.5 Ischemic Encephalopathy
- •8.3.5.1 Preterm Infant
- •8.3.5.2 Global or Diffuse Brain Oedema
- •8.3.6 Other applications of (C)DS:
- •8.3.7 Inflammation
- •8.3.7.2 Postnatal Inflammation
- •8.3.9 Cerebral Haemorrhage
- •8.3.10.1 Vascular Malformations
- •8.3.11 Cerebral Calcifications
- •8.4.1 Introduction
- •8.4.2 Haematoma
- •8.4.4 Skull Fracture
- •8.5 Additional Imaging
- •8.5.1 Plain Film
- •8.5.2 CT
- •8.5.3 MRI
- •8.5.4 Catheter Angiography
- •8.5.5 Additional Supporting Procedures
- •8.6.1 Introduction
- •8.6.2 Normal Findings
- •8.6.3 Sonographically Depictable Pathology
- •9.1 Introduction
- •9.2 Requisites
- •9.4 Indications
- •9.5 Normal Findings
- •9.6.1 Dysraphism
- •9.6.2 Other Associated Pathology
- •9.6.3 Other “Occult” Dysraphisms
- •9.7 Trauma
- •9.8 Tumours and Miscellaneous Others
- •9.10 Additional Imaging
- •10.1.1 Transducers
- •10.1.3 Typical Examinations
- •10.1.3.1 Cervical Lymph Nodes
- •10.1.3.2 Glands
- •10.1.3.3 Cervical Arteries
- •10.1.3.4 Cervical Veins
- •10.1.3.5 Intervention
- •10.2 Normal Findings
- •10.2.1 Lymph Nodes
- •10.2.2 Cervical Glands
- •10.2.2.1 Thyroid Gland
- •10.2.3 Other Cervical Soft Tissues
- •10.2.3.1 Muscles
- •10.2.3.2 Tonsils
- •10.2.3.3 Tongue
- •10.2.3.5 Larynx
- •10.2.4 Cervical Vessels
- •10.3 Pathologic Findings
- •10.3.1 Lymph Nodes
- •10.3.2.1 Malformations
- •Cervical Cyst
- •Dermoid Cyst
- •Duplication Cysts
- •Thymic Cyst
- •Cervical Ectopic Thymus
- •10.3.2.2 Tumours
- •Haemangioma
- •Lymphatic Malformation
- •Other Mesenchymal Tumours
- •Teratoma
- •Other Malignant Tumours
- •10.3.2.3 Abscess Formations
- •10.3.2.4 Traumatic Changes
- •Haematoma (Including Sternocleidomastoid Muscle “Haematoma”)
- •10.3.3 Thyroid Gland
- •10.3.3.1 Cystic Changes
- •10.3.3.2 Malformations
- •10.3.3.3 Inflammation
- •10.3.3.4 Other Conditions
- •Nodular Goitre
- •Amyloid Goitre
- •Adenoma/Carcinoma
- •10.3.4 Salivary Glands (Parotid, Sublingual, Submandibular Gland)
- •10.3.4.1 Inflammation
- •10.3.4.2 Cysts
- •10.3.4.3 Calcifications/Sialolithiasis
- •10.3.4.4 Tumours
- •10.3.5 Cervical Vessels
- •10.3.5.1 Arteriosclerosis
- •10.3.5.2 Dissection
- •10.3.5.3 Stenosis
- •10.3.5.4 Other Vascular Anomalies
- •11.1 Introduction
- •11.2.1 Transducers
- •11.2.2 Standard US Techniques
- •11.2.3 Patient Position
- •11.2.4 Sedation
- •11.4 Normal 2D Echocardiogram Findings
- •11.4.1 Parasternal Views
- •11.4.1.3 Apical Views
- •11.4.2 Subcostal Views
- •11.4.2.1 Sagittal Subcostal View
- •11.5 Other Techniques
- •11.5.1 M (Motion)-Mode Echocardiography
- •11.6 Special Echocardiographic Techniques
- •11.6.1 Transoesophageal Echocardiography (TEE)
- •11.6.2 Three-/Four-Dimensional (3D/4D) Echocardiography
- •11.6.3 Tissue Doppler Imaging (TDI)
- •11.6.4 Contrast-Enhanced US (ce-US/CEUS)
- •11.7 Normal Values
- •11.8 Pathologic Findings
- •11.8.1.1 Atrial Septal Defect (ASD)
- •11.8.1.2 Atrioventricular Septal Defects (AVSD)
- •11.8.1.3 Ventricular Septal Defects (VSD)
- •11.8.2.1 Aortic Valve Stenosis (AS)
- •11.8.2.2 Subaortic Stenosis (Sub-AS)
- •11.8.2.3 Supravalvular Aortic Stenosis
- •11.8.2.4 Aortic Coarctation (CoA)
- •11.8.2.5 Interrupted Aortic Arch
- •11.8.3.1 Isolated Pulmonary Valve Stenosis (PS)
- •11.8.3.2 Subvalvular Pulmonary Stenosis
- •11.8.3.3 Supravalvular Pulmonary Stenosis
- •11.8.4 Miscellaneous Congenital Heart Defects
- •11.8.4.2 Total Anomalous Pulmonary Venous Return (TAPVR)
- •11.8.4.3 Univentricular Heart (UVH)
- •11.8.4.4 Double Outlet Right Ventricle (DORV)
- •11.8.4.5 Ebstein Anomaly
- •11.8.4.6 Cor Triatriatum
- •11.9 Acquired Paediatric Heart Diseases
- •11.9.1 Cardiomyopathies (CMP)
- •11.9.1.1 Hypertrophic CMP
- •11.9.1.2 Hypertrophic Obstructive CMP (HOCMP)
- •11.9.1.3 Dilated (Congestive) CMP
- •11.9.1.4 Restrictive CMP
- •11.9.2 Acute Myocarditis
- •11.9.3 Acute (Infective) Endocarditis
- •11.9.4 Pericarditis/Pericardial Effusion
- •11.9.5 Kawasaki Disease
- •11.9.6 Intracardiac Thrombi
- •11.9.7 Cardiac Tumours
- •11.11 Complementing Investigations
- •11.12.1.1 Typical Orientating Examination
- •11.12.1.2 Typical Clinical Queries
- •12.1 Requisites
- •12.1.1 Transducers
- •12.1.2 Positioning
- •12.1.3 Indications
- •12.2 Normal Findings
- •12.2.1 Chest Wall
- •12.2.2 Breast
- •12.2.3 Pleural Space
- •12.2.4 Diaphragm
- •12.2.5 Lung
- •12.2.6 Mediastinum
- •12.2.6.1 Anterior Mediastinum/Thymus
- •12.2.6.2 Middle Mediastinum
- •12.2.6.3 Posterior Mediastinum
- •12.2.7 (Colour) Doppler Sonography
- •12.2.8 Contrast Enhanced US (ce-US)
- •12.3.2 Congenital Malformations
- •12.3.3 Traumatic Changes
- •12.3.4 Chest Wall Tumours
- •12.3.4.1 Lymphangioma (Venolymphatic Vascular Malformation)
- •12.3.4.2 Lipoma
- •12.3.4.3 Fibroma/Neurofibroma
- •12.3.4.4 Other Tumours
- •12.3.5 Breast
- •12.3.6 Miscellaneous Other Applications
- •12.4.1 Pneumothorax
- •12.4.2 Pleural Effusion
- •12.4.2.1 Empyema
- •12.4.3 Other Pleural Pathology
- •12.5.1 Diaphragmatic Hernia
- •12.5.2 Diaphragmatic Motion Disturbance
- •12.6 Lung Pathology
- •12.6.1 Pneumonia
- •12.6.2 Lung Abscess
- •12.6.3 Atelectasis
- •12.6.5 Sequestration
- •12.6.6 Congenital Cystic Adenomatoid Malformation (CCAM)
- •12.6.7 Cysts
- •12.6.8 Infarction
- •12.8 Additional Imaging
- •13.1 Introduction
- •13.2.1 Preparation
- •13.2.2 Positioning
- •13.2.3 Transducers
- •13.3 Liver
- •13.3.2 Standard Planes
- •13.3.3 Normal Findings
- •13.3.3.1 Structure
- •13.3.3.2 Ligaments
- •13.3.3.3 Hepatic Veins (HV)
- •13.3.3.4 Portal Vein (PV)
- •13.3.3.5 Hepatic Artery (HA)
- •13.3.3.6 Gall Bladder
- •13.3.3.7 Common Bile Duct
- •13.3.3.8 Intrahepatic Bile Ducts
- •13.3.3.9 Doppler Findings
- •Situs Inversus (Abdominalis)
- •Butterfly or Midline Liver
- •13.3.4.2 Inflammatory Conditions
- •Hepatitis
- •Liver Abscess
- •Granulomatous Disease
- •13.3.4.3 Other Parenchymal Liver Disease
- •Fatty Liver/Steatosis
- •Liver Congestion
- •Liver Fibrosis
- •Cirrhotic Liver
- •Portal Hypertension
- •Vascular Malformations
- •Hepatic Vein Thrombosis/Occlusion/Stenosis
- •Portosystemic Shunts
- •13.3.4.5 Liver Trauma
- •Liver Haematoma
- •Contusion
- •Laceration
- •Haemobilia
- •Associated Diaphragmatic Injury
- •Liver Infarction
- •Additional Imaging
- •13.3.4.6 Space-Occupying Liver Lesions
- •Simple Cysts
- •Complicated Cysts
- •Liver Calcifications
- •Intrahepatic Gas
- •Haemangioma
- •Mesenchymal Hamartoma
- •Focal Nodular Hyperplasia (FNH)
- •Hepatic Adenoma
- •Fatty Tumours
- •Hepatoblastoma
- •Hepatocellular Carcinoma
- •Hepatic Sarcomas
- •Metastasis
- •Proliferative Disorders
- •Additional Imaging
- •13.4.1 General Findings
- •13.4.2.1 Intrahepatic Gall Bladder
- •13.4.2.3 Choledochal Cyst
- •13.4.3 Biliary Tract Diseases
- •13.4.3.1 Aerobilia
- •13.4.3.2 Cholestatic Changes/Inspissated Bile/Gallstone
- •13.4.3.3 Sclerosing Cholangitis
- •13.4.3.5 Tumour-like Conditions
- •Polyps
- •Tumours
- •13.4.3.7 Additional Imaging
- •13.5.1 Pretransplant US
- •13.5.1.1 Recipient Evaluation
- •13.5.2 Intraoperative US
- •13.5.3 Postoperative Assessment
- •13.5.4 Typical Complications
- •13.6 Spleen
- •13.6.1 Requisites
- •13.6.2 Positioning
- •13.6.3 Indications
- •13.6.5 Normal Anatomy
- •13.6.6 Normal Variants
- •13.6.6.1 Splenunculus (Accessory Spleen)
- •13.6.7 Malformations
- •13.6.7.1 Asplenia
- •13.6.7.2 Polysplenia Syndrome
- •13.6.7.3 Wandering Spleen
- •13.6.8 Splenomegaly
- •13.6.9 Trauma
- •13.6.10 Splenic Infarction
- •13.6.11.1 Cysts
- •13.7 Pancreas
- •13.7.1 Requisites
- •13.7.2 Indication
- •13.7.4 Normal Findings
- •13.7.5.1 Annular Pancreas
- •13.7.5.2 Pancreas Divisum
- •13.7.6 Inflammation: Pancreatitis
- •13.7.6.1 Oedematous or Reactive Pancreatitis
- •13.7.6.2 Haemorrhagic or Necrotising Pancreatitis
- •13.7.6.3 Chronic Pancreatitis
- •13.7.7 Trauma
- •13.7.8 Space-Occupying Lesions
- •13.7.8.1 Cysts/Pseudocysts
- •13.7.8.2 Tumours
- •13.7.10 Additional Imaging
- •13.8.1 Abdominal Vessels
- •13.8.1.1 Positioning
- •13.8.1.2 Transducers
- •13.8.1.4 US Findings
- •13.8.2 Vascular Pathology
- •13.8.2.1 Thrombosis/Occlusion
- •13.8.2.2 Pelvic Congestion Syndrome
- •13.8.2.3 Mid-Aortic Syndrome
- •13.8.2.4 Retroaortic Left Renal Vein: Nutcracker Syndrome
- •13.8.2.9 Complementing Imaging
- •13.8.3 Retroperitoneal Soft Tissues
- •13.8.3.1 Lymph Nodes
- •13.8.3.2 Retroperitoneal Tumours
- •13.8.3.3 Abdominal Wall
- •14.1 Stomach
- •14.1.1 Requisites
- •14.1.2.1 Access
- •14.1.3 Normal Findings
- •14.1.4 Normal Variants
- •14.1.5 Malformations
- •14.1.5.1 Microgastria
- •14.1.5.2 Pyloric Atresia
- •14.1.5.3 Congenital Hiatal Hernia
- •14.1.6 Pathologic Findings
- •14.1.6.1 Gastro-Oesophageal Reflux (GOER)
- •14.1.6.2 Hypertrophic Pyloric Stenosis (HPSt)
- •14.1.6.3 Other Stomach Conditions
- •14.2 Bowel
- •14.2.3 Normal US Findings
- •14.2.4 Pathology
- •14.2.4.1 Congenital Anomalies
- •14.2.5 Acquired Obstructive Pathology
- •14.2.5.1 Meconium Ileus
- •14.2.5.2 Midgut Volvulus
- •14.2.5.3 Sigma Volvulus
- •14.2.5.4 Hernia
- •14.2.5.5 Intussusception
- •14.2.6 Inflammatory Conditions
- •14.2.6.1 Necrotising Enterocolitis (NEC)
- •14.2.6.2 Gastroenteritis
- •14.2.6.3 Henoch–Schönlein Purpura
- •14.2.6.4 Appendicitis
- •14.2.6.5 Crohn’s Disease
- •14.2.6.6 Colitis
- •14.2.6.7 Other Inflammatory Bowel Conditions
- •14.2.6.8 Bowel Trauma
- •14.2.7 Mesentery
- •14.2.7.1 Mesenteric (Peritoneal) Masses
- •14.2.7.2 Abscesses
- •14.2.7.3 Twisted Appendices Epiploica
- •14.2.8 Mesenteric Lymph Nodes
- •14.2.9 Free Intraperitoneal Air
- •14.2.10 Free Intraperitoneal Fluid: Ascites
- •14.2.11 Mesenteric Vessels
- •15.1 Requisites
- •15.1.1 Indications
- •15.1.2 Preparation
- •15.1.3 Transducers
- •15.1.4 Positioning
- •15.1.5.1 Diuretic US
- •15.1.6 Contrast-Enhanced Voiding Urosonography (ce-VUS)
- •15.2 Normal Findings
- •15.2.1 Bladder
- •15.2.2 Kidney
- •15.2.2.1 Normal Variants
- •Duplex Kidney
- •Ectopic Kidneys
- •Renal Agenesis
- •15.3.1 Congenital Conditions
- •15.3.1.1 Dysplasia/Hypoplasia
- •15.3.1.2 Cystic Renal Disease
- •Inherited/Congenital Cystic Disease
- •Acquired Cystic Kidney Disease
- •Urinary Tract Dilatation (UTD) or Pelvicalyceal Dilatation/Distention (PCD)
- •Pelvi-ureteric Junction Obstruction (PUJO)
- •Uretero-Vesical Junction Obstruction (UVJO)/Obstructive Megaureter (POM/MU)
- •Posterior Urethral Valve (PUV)
- •Vesico-Ureteric Reflux (VUR)
- •Secondary Obstruction
- •15.3.2 Inflammatory Renal Parenchymal Conditions
- •15.3.2.1 Pyelitis
- •15.3.2.2 Acute Pyelonephritis (aPN)/Interstitial Nephritis
- •15.3.2.4 Scarring
- •15.3.2.5 Tuberculosis
- •15.3.2.6 Xanthogranulomatous Pyelonephritis
- •15.3.2.7 Glomerulonephritis/Nephrotic Syndrome
- •15.3.3 Vascular Conditions
- •15.3.3.1 Renal Artery Stenosis
- •15.3.3.2 Arteriovenous Fistula (AVF)
- •15.3.3.3 Infarction
- •15.3.3.4 Renal Vein Thrombosis
- •15.3.4 Nephrocalcinosis
- •15.3.5 Urolithiasis
- •15.3.6 Other Important Renal Parenchymal Disease
- •15.3.6.1 Haemolytic Uremic Syndrome (HUS)
- •15.3.6.2 Glomerulonephritis/Nephrotic Syndrome
- •15.3.6.3 Scars, Cirrhotic Kidney
- •15.3.7 Renal Failure (RF)
- •15.3.8 Renal/Urinary Tract Trauma
- •15.3.9 Renal Tumours
- •15.3.9.1 Benign Tumours
- •15.3.9.2 Pre- or Semi-Malignant Tumours
- •15.3.9.3 Malignant Tumours
- •15.4.1 Renal Biopsy
- •15.4.2 Drainage/Nephrostomy
- •15.4.3 Postoperative Imaging
- •15.4.3.1 After VUR Treatment
- •Cystoscopic Treatment
- •Antireflux Surgery
- •15.4.3.2 Findings after Pyeloplasty
- •15.4.3.3 After Various Interventions
- •15.5 Renal Transplant
- •15.5.2 Pathologic US Findings
- •15.6.1 General Remarks
- •15.6.2 Typical Normal US Finding
- •15.6.3 Pathologic Findings
- •15.6.3.1 Adrenal Gland Haemorrhage
- •15.6.3.2 Inflammatory Condition
- •15.6.3.3 Tumours
- •Adrenal Cysts
- •Adrenal Adenoma
- •Neuroblastoma
- •Ganglioneuroma
- •Phaeochromocytoma
- •Adrenal Carcinoma
- •15.7.1 Requisites
- •15.7.2 Pathologic Findings
- •15.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
- •15.7.2.2 Polyps
- •15.7.2.3 Bladder Tumours
- •15.7.2.4 Calcification in/of Bladder
- •15.7.2.5 Ureterocele
- •15.7.2.6 Persisting Urachus
- •15.7.2.7 Megaureter
- •15.7.2.9 Inflammation
- •15.7.2.10 Traumatic Changes
- •15.7.2.11 Vesico-Ureteric Reflux
- •15.7.3 Paravesical Changes
- •15.7.3.1 Abscess Formations
- •15.7.3.3 Cystic Perivesical Structures
- •15.8.1 US Technique
- •15.8.2 Normal Findings
- •15.8.3 Common Pathologic Findings
- •15.8.3.1 Hydrocele
- •15.8.3.2 Undescended Testes
- •15.8.3.3 Varicocele
- •15.8.3.6 Microlithiasis
- •15.8.4 Inflammation—Orchitis, Ependymitis
- •15.8.5 Scrotal Trauma
- •15.8.6 Torsion
- •15.8.6.2 Inguinal Hernia
- •15.8.7 Testicular Tumours
- •15.9 Female Genitals
- •15.9.1 Indications
- •15.9.2 Requisites
- •15.9.3 Transducers
- •15.9.5 Normal Findings
- •15.9.5.1 Sonogenitography
- •15.9.6 Pathologic Findings
- •15.9.6.1 Congenital Malformations
- •Vaginal Atresia
- •Vaginal Fistula
- •Other Vaginal Malformations
- •Vaginal Aplasia
- •Uterine Malformations
- •Ovarian Malformations
- •Cysts
- •Teratoma
- •Other Genital Tumours
- •Rhabdomyosarcoma
- •15.9.6.4 Traumatic Changes
- •Ovarian Torsion
- •Pregnancy
- •16.1 General Remarks
- •16.2 Examination Technique
- •16.2.2 Modified Graf Classification (Rosendahl)
- •16.3 Normal Anatomy
- •16.3.2 Rosendahl Modification
- •16.3.3 Normal Findings During Harcke Investigation
- •16.5 Pathologic Findings
- •16.6.1.1 Capsular Thickening
- •16.6.1.2 Joint Fluid/Effusion
- •16.6.2 Hip Osteoarthritis
- •16.6.4 Perthes Disease
- •17.1.2 Typical Normal Findings
- •17.1.3 Pathologic Findings
- •17.1.3.1 Fracture
- •17.1.3.2 Joint Effusion
- •17.1.3.3 Arthritis
- •17.1.3.4 Trauma
- •17.1.3.5 Cysts
- •17.1.3.6 Inflammation
- •17.1.3.7 Neoplasia
- •17.2 Other Small Part Applications
- •17.2.1 General Remarks
- •17.2.2 Foreign Bodies

3 (Color) Doppler US: Theory, Artefacts, Typical Applications inChildhood
45
• Combination of aCDS with split/double image technique, extended eld of view/
panoramic US (see above) or integration of aCDS into 3D-/4DUS possible—
vessels can be visualised over signicant longer distances or even with rather
tortuous and complex anatomy (Fig.3.5a, b).
3.1.2.6 Other Flow-Sensitive US Techniques
Time domain or (colour) velocity imaging depicts motion of single reectors
between consecutive images by using extremely high spatial and temporal resolution (subtraction technique). This allows motion depiction, as individual structures
are imaged at different times at different locations.
Promising method—particularly with regard to sensitivity, angle dependency
and measurement accuracy; works at far less sound pressure than aCDS with better
frame rates (but sometimes restricted penetration).
Note Presently only few vendors offer this technique in some dedicated devices
(e.g. B-ow by GE) (Fig.3.6), but more are coming up.
3.1.2.7 Important Parameters andMeasurements (Fig.3.7)
• V
syst.max.
=V
=maximal systolic ow velocity—only to be measured after angle
syst
correction.
• V
end diast.
=V
=maximum end-diastolic ow velocity—measurement only after
diast
angle correction.
• TAV—time average velocity; weighted mean velocity parameter that sums up
velocities of all particles within sample volume over dened cycle. Only correct
Fig. 3.5 3DUS with integrated aCDS. (a) Rendered image of a 3DUS—aCDS acquisition of a
neonatal brain demonstrating a large vein of Galen AVM with its main feeders and a short section
of the enlarged draining vein (not entirely depicted due to scale settings during acquisition). (b)
3DUS with included CDS data of a soft tissue vascular malformation, acquisition from dorsal
approach. Three orthogonal sections and rendered CDS-weighted view that superiorly demonstrates marked vascularity of lesion

46
ab
Fig. 3.6 Non-Doppler ow imaging techniques: (a) Basic power Doppler image of a neonatal
kidney (preterm, free breathing, tachypnoea, circulatory impairment due to sepcticaemia) demonstrates a rather patchy and clumsy appearance of peripheral renal vasculature. (b) B-ow of the
same kidney delineates individual peripheral vessels much better in spite of peripherally impaired
perfusion—particularly in the near eld
M. Riccabona
Fig. 3.7 Doppler measurements and calculations. Typical Doppler high (a) and low (b) resistance
ow pattern with respective relevant measurements. Abbreviations: V
low line), V
mean velocity (orange line), t 0, t=time of measurement
mean
if angle correction possible, vessel position stable throughout entire measurement cycle and proper placement of sample volume throughout feasible.
• TAMX—time average maximum velocity; mean maximum ow velocity
throughout measurement cycle—angle correction necessary.
RI—resistance (or resistive) index (Pourcelot index)—angle independent param-
eter that calculates relation between systolic and diastolic maximum velocity.
Describes resistance or impedance but also inuenced by many other factors.
Equation: RI=V
syst
−V
diast/Vsyst
• PI—pulsatility index (Gosling index); describes ow details throughout entire
systolic-diastolic cycle, very sensitive towards even minor changes within ow
prole—but extremely depends on accurate angle correction.
maximum velocity (yel-
max

3 (Color) Doppler US: Theory, Artefacts, Typical Applications inChildhood
47
Equation: PI=V
syst
−V
/TAM; X
diast
• Q—volume ow (mL/min)—different parameters and calculations used:
– Q
=TAV×A (A—section area of vessel—if planimetrically measured or
time
use equation for A from below).
Note: New 4D quantitative methods (e.g. QIBA) are being developed, but yet
still not routinely available (though some companies are getting close, e.g.
Phillips)
– Q
=VTI×A (A=π x D/22), D—diameter=2 R, VTI—velocity time
per systoly
integral=integral of systolic velocities, i.e. area under the curve dened by
maximum velocity throughout cycle).
– Simplied equation: Q (mL/min)=TAV(m/s)×D2(mm)×47.1 (correction
factor).
Note: Oblique vessel sections cause signicant errors. Flow volume measurements depend on adequate angle correction and particularly on accurate measurement of cross-sectional area and/or diameter of vessel.
• AI (or ACCI)—acceleration index; important for evaluation of stenosis. Describes
rise of systolic ow velocity, i.e. time from beginning of systole until reaching V
syst.max
3.2 Artefacts in(Colour) Doppler Sonography
3.2.1 Aliasing
Confusing display of high velocities (beyond the Nyquist border) or wrong velocity
scale settings; the part of systolic velocity too high for scale/beyond Nyquist border
added on opposite side of scale or encoded in opposite colour (Fig.3.8).
.
Fig. 3.8 (a) CDS of a PDA; the sparkling colour signals indicate aliasing due to turbulent and
high-velocity ow; the maximum systolic velocity is higher than depictable by the respective
colour map setting/the Nyquist border (i.e. applicable pulse repetition frequency). (b) Flow graph
for spectral analysis of a PW or CW Doppler trace: High-velocity systolic ow, cannot be properly
displayed on the screen due to missing correction of the baseline and the high ow velocity; the
respective part of the systolic ow is represented by spectra coming into the image from below and
reaching up to and even above the baseline

48
M. Riccabona
3.2.2 Spectral Broadening
Indicates turbulent ow, for example, with stenosis or vessel wall pathology/
irregularity:
• Same phenomenon articially caused by inadequately high gain (recognised
by increased background noise on display of duplex trace or colour noise
on image).
3.2.3 Sample Volume Artefact
The individually adaptable size of individual measurement can cause errors.
If sample volume is positioned incorrectly, may lead to incomplete measure-
ments or signicant artefacts:
• A too large sample volume includes pulsation from vessel wall.
• A too small sample volume depicts only central fast ows, whereas more peripheral slower and potentially turbulent ow not included.
3.2.4 Filtering Artefacts
If lters are set too high, low velocities are not displayed even if present—may
mimic pathology (e.g. missing antegrade diastolic ow).
3.2.5 Scaling Problems
Incorrect measurements can be caused by inadequate adaptation of scale or
baseline.
3.2.6 Gain-Induced Errors
If gain is set too low, existing ow may not be depicted.
If gain is set too high, articial turbulences may be simulated.
3.2.7 Angle Correction
Inadequate angle correction may cause signicant errors in measurements, e.g.
caused by poor vessel delineation due to tortuosity in axial or oblique plane not or
uncorrectable in imaging plane.
Furthermore, high Doppler angles cause inaccuracies (see also Table3.1).

3 (Color) Doppler US: Theory, Artefacts, Typical Applications inChildhood
49
3.2.8 Motion Artefact
Particularly a problem with aCDS.Motion can cause colour signals (e.g. breathing, pulsating tissue, adjacent peristalsis or organ movement)—not to be mistaken for real ow.
3.2.9 Twinkling Artefact
Reverberating structures of strong echogenicity that undulate in sound eld; these
and not motion create sparkling colour signals—useful for depiction of concrements/calcications or solid deposits (see Fig.3.9c, d).
Note Not all concrements cause twinkling—the artefact very much depends on
nature, size and composition of concrement, transducer frequency, focus setting,
equipment used as well as on gain, lter and scale settings. Can also be seen with
air, resembling reverberation artefacts on grey scale US—to be identied by typical
spikes on duplex trace.
Fig. 3.9 Examples for CDS artefacts. (a, b) CDS mirror artefact. CDS of the proximal IVC (tran-
shepatic sagittal view) at junction with diaphragm: echogenic border (caused by air in the lung)
causes mirroring of vessel colour display (encoded in blue) into intrathoracic cavity mimicking an
aberrant vessel (displayed in red). (c, d) Twinkling artefact—grey scale and CDS. Axial view,
kidney of an infant: small echogenic spot of indicating a papillar precipitation that causes twinkling non-directional colours signals (“twinkling sign”)

50
M. Riccabona
3.2.10 Others
A variety of artefacts as described previously on grey scale US can also occur on
Doppler, such as mirroring (Fig.3.9).
3.3 How toPerform (Colour) Doppler Investigations
Some special aspects need to be considered in equipment setting and transducer
handling.
Note Doppler US uses signicantly higher energy, therefore particularly in vulner-
able areas, investigation should be as short as possible; always observe TI values.
• Try to use lowest possible output energy after pre-adapting other parameters
such as scale/velocity, lters, sample volume size and update rate before starting
Doppler tracing.
• Usually Doppler investigations are performed at lower frequency than grey scale
imaging—therefore usually multifrequency transducers are used for CDS (e.g.
grey scale 7MHz, Doppler 5 or 4MHz).
• Initially images are optimised on grey scale, then targeted vessel is focused trying to optimise position and imaging for Doppler conditions—then Doppler is
activated to improve vessel delineation and speed up orientation.
• After further image optimisation (adapting focus to relevant area), zoom, etc. can
be applied to further improve image and consequently allow for adequate
measurements.
• Thereafter, cursor with sample volume is placed in vessel, sample size is optimised—only then triplex or duplex mode is activated. Again, try to avoid unnecessary high output gain; adjust receive gain, scale, ltering and all other
parameters.
• For measurements, Doppler trace of at least several consecutive cycles should be
obtained—without impairing background noise.
• Take measurements afterwards on frozen image to avoid unnecessary tissue
exposure/high sound pressure.
3.3.1 Limitations
• Inaccessible areas for US, structures interfering with access such as interposed
air or calcied structures.
• High Doppler angles.
• Signicant motion.
• Furthermore, extremely high velocities can cause problems (“Nyquist border”=beyond the scale the pulse repetition frequency allows for).

3 (Color) Doppler US: Theory, Artefacts, Typical Applications inChildhood
51
3.3.2 Interpretation
For reading colour/duplex-Doppler images, profound knowledge about pathophysiology and impact on perfusion/resistance is essential. Several parameters impact
spectral Doppler traces (Fig.3.10):
• Diameter of vessel: the larger the diameter, the more laminar ow exists, particularly within central lumen.
• Rheologic composition of blood: depends on concentration of corpuscular particles as well as composition of uids.
Fig. 3.10 Schematic drawing of various Doppler ow proles. Typical ow pattern encountered
in various conditions, with respect to site of relevant pathology in relation to point of measurement
(before, at, after lesion) and cardiac function. RI (restive index) changes indicated. 1 normal, 2
volume overload, increased cardiac output, 3 reduced cardiac output, 4 measurement after stenosis,
5 measurement at stenosis, 6 measurement before area of diminished resistance/shunt, 7 measurement before area of increased resistance, stenosis, perfusion impairment, 8 measurement in area of
increased resistance/perfusion impairment, 9 measurement close to occlusion/perfusion stop, 10
measurement after shunt

52
• Overall blood volume as well as cardiac function impact ow velocities and ow
proles—even in peripheral vessels. Furthermore, changes of vessel wall impacting diameter and elasticity affect ow prole.
• Caliber variations impact ow spectrums—not only at site of stenosis but usually
if haemodynamically signicant, up- and downstream as well. Can also be
caused by transducer pressure inducing articial compression.
• Additional aspect: peripheral resistance especially impacts diastolic ow.
M. Riccabona
3.4 Three- andFour-Dimensional US (3D-/4DUS)
3.4.1 Physics andTechniques
Several different techniques used for acquiring 3DUS data:
• Originally series of 2D images combined with some position information for
reconstructing 3D data set. Position information either derived from some sort of
positioning device (optical-, acoustic-, electromagnetic sensors, mechanical
positioning devices, etc.) or from estimated transducer shift, using information
derived from extended view—like vector analysis-based calculation.
• Presently most commonly used: 3D transducers—scan heads that have integrated motor which mechanically moves scan head through acquisition eld thus
dening each individual plane by motor sweep speed.
• Most modern techniques—matrix transducers that have 2D crystal matrix; allows
for simultaneous acquisition of real volume by electronic steering.
After data acquisition and reconstruction of 3D volume—data viewed in multi-
ple displays:
• Multi-axial sections.
• CT-like tomographic parallel sections.
• Any kind of reconstruction as with CT and MRI.
• Various rendering algorithms are applicable—to visualise and extract volume
information difcult to display in 2D planes (e.g. tortuous structures, cavities
and surfaces).
Repeated update of such 3D acquisitions allows for lm-like visualisation—
hence called 4DUS, with time being the fourth dimension. Particularly useful when
analysing motion-depending phenomena of structures only properly depicted by
3DUS either due to inaccessible plane for conventional 2DUS or surface information.
3.4.2 Typical Paediatric 3DUS Applications
3.4.2.1 Neonatal Neurosonography
Using open fontanel and dedicated 3DUS transducers, practically the entire neonatal brain is covered in one or two 3D volumes. Standard sections comparable to CT

3 (Color) Doppler US: Theory, Artefacts, Typical Applications inChildhood
53
and MRI reconstructed, particularly crucial (axial, coronal) planes (often not available on 2DUS) retrievable from data set, valuable not only for documentation but
also for:
• DDx—particularly with cystic structures and anatomic correlation (Fig.3.11).
• Analysis of complex and tortuous structures or hydrocephalus (Fig.3.12).
• Standardised assessment of extra-axial uid space, cerebral ventricles, major cerebral vessels, etc. Furthermore—provided sufcient extra-axial uid around brain—
brain surface viewing can be attempted opening up completely new eld for
research/US diagnostic potential (migration/gyration disorders, etc.) (Fig.3.13).
3.4.2.2 3DUS oftheKidney
Particularly useful in kidneys with pelvicalyceal distention. Using segmentation
algorithms, real renal parenchymal volume (after deduction of dilated collecting
Fig. 3.11 Neonatal brain
3DUS: improved DDx and
conspicuous viewing by
3DUS.Tomographic
display: CT-like
demonstration after axial
reconstruction of an
intracranial (arachnoid)
cyst that obviously does
not connect to the only
slightly dilated
supratentorial ventricles
Fig. 3.12 Neonatal brain
3DUS: hydrocephalus.
Three orthogonal views
and segmented-inverted
rendered view of dilated
ventricles (right lower box)
in a baby with
supratentorial
hydrocephalus

54
Fig. 3.13 Brain 3DUS in a preterm: brain surface assessment. This
surface- weighted rendered view of brain surface in a preterm baby
nicely demonstrates jet reduced and physiologically immature gyration
Fig. 3.14 3DUS kidney for volume calculation: two views of a stepwise segmentation process.
(a) Entire kidney has been manually extracted from data volume, with demarcation of semiautomatically segmented dilated collecting system (threshold and grey scale inversion approach,
collecting system seen white). (b) After deduction of colleting system, only renal parenchyma
left—volume can then be calculated, and thus renal parenchymal volume calculation (including
split renal size estimates) can be performed even in hydronephrotic kidneys
M. Riccabona
Fig. 3.15 3DUS in pelvicalyceal dilatation. Three orthogonal and segmented-inverted rendered
view of dilated collecting system (right lower box) in a baby with pelvi-ureteric junction obstruction
system) can be calculated, split renal volume can be estimated—reliably offers
essential information in patients with obstructive uropathy, particularly valuable
during follow-up (Fig.3.14):
• Using threshold-based and inversion-rendering techniques, conspicuous IVU- or
MRU-like display of dilated collecting system and its anatomy is provided
(Fig.3.15).
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