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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

118
M. Riccabona
Fig. 8.5 Planimetric measurement of cerebellar
size. Cerebellum (dotted line) outlined for
planimetry—age adapted normal values, see
Table8.1
Table 8.1 Cerebellar size in preterm and term neonates
Gestational age (week)
26 600 0.75
28 820 1.30
30 1330 1.95
32 1580 2.43
34 1900 2.66
36 2220 3.18
38 2840 3.56
40 3100 3.98
Body weight (g)
Cerebellar area (cm2)
– Every abnormality documented in two orthogonal planes, reproducible mea-
surements helpful.
– Additional views helpful: brain surface with linear transducer, mastoid view
for posterior fossa and CDS images with respective duplex trace (ICA, ACA,
MCA, circle of Willis, BA, major veins).
8.2 Normal Findings
8.2.1 Transfontanellar Access
Ventricular System
• Slim lateral ventricles with symmetric conguration, <10mm diameter at level
of foramen of Monro.
• Normal CSF: without any echoes.
• Choroid plexus: echogenic structure partially outlining ventricle, in posterior
parts oating within CSF.
• Ventricular system used as landmark for most parts of brain.

8 Neurosonography inNeonates, Infants andChildren
119
Other Physiologic Cavities to Visualise
• Various cisterns.
• Various embryologic remnants such as cavum septi pellucidi, cavum vergae,
cavum velum interpositum.
• Extra-axial CSF space (interhemispheric ssure).
Brain Parenchyma
• More or less homogeneous, of medium echogenicity, slight difference between
darker cortex and more echogenic white matter, identied echogenic sulci (may
be inverted or masked with immaturity, oedema, myelination disorders etc.).
• Basal ganglia and internal capsule identied by different echogenicity with highresolution transducers.
• Major vessels appear as echogenic pulsating tubular or nodular structures.
8.2.2 Alternate Access Findings
Image appearance varies with access (e.g. transtemporal view); usually important
basal and central structures can be easily differentiated:
• Lateral ventricles, foramen of Monro, third and fourth ventricle, connecting
aqueduct of Sylvius, crura cerebri, major parts of basal ganglia, tentorium, parts
of cerebellum, basal vessels and contralateral extra-axial CSF spaces.
• Mastoid access: occipital horn with choroid plexus, adjacent parenchyma
(Fig.8.6) and cerebellum.
Fig. 8.6 Mastoid access with sector transducer. (a) Posterior fossa, axial view; note large cistern
(↔). (b) Axial view at posterior horn (→) of lateral ventricle with haemorrhage (++) and respective plexus

120
M. Riccabona
8.2.3 Colour Doppler Sonography (CDS)
Transfontanellar
• Anterior cerebral artery (ACA) and its branches (particularly the pericallosal)
and basilar artery (BA)—best seen in sagittal sections (Fig.8.7a, c).
Fig. 8.7 Major cerebral vasculature on aCDS. (a) Schematic drawing how to access the ACA/
pericallosal artery and the basilary artery (BA) in a sagittal section. (b) Schematic drawing how to
access in a coronal section. (c) Sagittal midline section, aCDS: BA, ICA, ACA and branches seen,
duplex sample positioned in pericallosal artery. (d) Parasagittal section CDS depicts the ICA when
entering into intracranial portion. (e) Coronal CDS demonstrates both ICA and the branching into
MCA and ACA. (f) CDS, coronal section tilted occipitally: major veins/venous sinus of posterior
fossa depicted (displayed in blue) and branches of PCA. (g) CDS in sagittal section to evaluate
midline veins, particularly the superior sagittal sinus. Abbreviations: (a)CDS (amplitude) coded
colour Doppler sonography, BA basilar artery, ICA internal carotid artery, ACA anterior cerebral
artery, MCA middle cerebral artery and PCA posterior cerebral artery

b
8 Neurosonography inNeonates, Infants andChildren
121
• Circle of Willis with its major feeding arteries and draining veins—best seen in
coronal section (Fig.8.7b, e).
• Internal carotid artery (ICA)—in parasagittal or coronal section (Fig.8.7b, d, e).
Note In patients who need cannulisation of CCA (e.g. for ECMO) or after CCA
injury, visualisation of anterior communicating artery is particularly important—if
seen, it indicates sufcient collateralisation of affected ACA area. Liberally use
(a) CDS, complemented by spectral analysis in relevant vessels.
Transtemporal Dopplersonography
Most vessels of circle of Willis are visible (Fig.8.8a), particularly:
• Middle cerebral artery (MCA), proximal part of ACA (A1-segment).
• Proximal part of posterior cerebral artery (PCA), posterior and anterior communicating arteries.
• Depiction of (proximal) ICA, distal ACA and BA difcult or impossible.
• This view used for transcranial ow evaluation (Fig.8.8b).
Venous System
Most veins visible and better seen from transfontanellar access (Fig.8.7f, g), for
example:
• Superior sagittal sinus, inferior sagittal sinus, sinus conuence (torcular herophili), vein of Galen and sigmoid and transverse sinus.
• Large sinus of posterior fossa—additionally use mastoid or transtemporal
approach (Fig.8.8c).
a
Fig. 8.8 (a) CDS—transcranial/transtemporal access (TCI). (a) Major arteries of circle of Willis
depicted by aCDS. (b) The TCI view used to place sample gate for spectral analysis with a normal
bidirectional arterial ow pattern from left and right MCA in the lower part of the image. (c) CDS
on TCI/posterior fossa: veins/sinus of posterior fossa can be assessed
c

122
M. Riccabona
Note For assessment of large veins, transducers with sufcient penetration at lower
frequencies may be necessary and ow settings have to be adapted to low ow
velocities.
Measurements
Arterial ow velocities as well as RI vary with age, but also with respiration, PCO2,
intrathoracic pressure (crying, ventilation, etc.), cardiac function, heart rate, etc.
Cerebral autoregulation only intact in mature healthy brain—then peripheral vessels
show less dependent ow variations. General rule:
• Flow velocities increase with age, RI decrease with age (in childhood).
• Respiratory variation typical of venous ow may persist.
Preterms: ow velocities 20–40cm/s, RI=80–90%.
Neonates: ow velocities 40–50cm/s, RI=75–80% (see Table8.2).
Older Neonates and Infants Assessed by transtemporal access. Flow velocities
increase; RI decreases to 60–70%, eventually reach adult values by end of rst year.
Physiologic decrease of arterial diastolic velocity with consequent elevated RI values in patients with persistent ductus arteriosus (PDA) or anaemia (Table8.3).
Functional Investigations
• Changes in ow spectrum, velocities and indices are observed with head positioning, particularly important for depicting infants at risk for sudden infant
death syndrome.
Table 8.2 Brain: Normal values for ow velocities (cm/s) and Doppler indices in ACA, ICA and
BA in newborns
ACA BA
Vs 42+15 41+16 50+15
Ves 19+8 18+7 19+7
Ved 11+5 11+4 11+4
TAV 13+5 12+5 14+4
TAMX 21+9 19+7 22+6
RI 0.73+0.08 0.72+0.09 0.77+0.08
PI 2.7+0.9 2.7+0.7 3.0+0.8
Adapted from Deeg KH (1989) Zerebrale Dopplersonographie im Kindesalter. Springer/Heidelberg,
Berlin/New York; Deeg KH, Rupprecht T (1989) Pulsed Doppler sonographic measurement of normal
values for the ow velocities in the intracranial arteries of healthy newborns. Pediatr Radiol 19:71–78
Abbreviations: ACA anterior cerebral artery, BA basilar artery, ICA internal carotid artery, PI
Pulsatility Index (Vs-Ved/TAV), RI Resistance Index (Vs-Ved/Vs), TAMX time average maximal
velocity, TAV time average ow velocity, Ve d end-diastolic velocity, Ves end systolic velocity and
Vs maximal systolic velocity
ICA

8 Neurosonography inNeonates, Infants andChildren
123
Table 8.3 Brain: Normal values for ow velocities and Doppler indices on TCI-Doppler investigations
Age
1–2.9years 3–5.9years 6–9.9years 10–17.9Jyears Adults
Vs (cm/s) MCA 124±10 147±17 143±13 129±17 110±28
Flow velocity Artery
ICA 118±24 144±19 140±14 125±18
ACA 81±19 104±22 100±20 92±19 79±21
ICA (siphon) 114±21 138±14 132±17 120±21
PCA1 67±18 84±20 82±11 75±16 71±16
BA 71±6 88±9 85±17 68±11
Ved (cm/s) MCA 65±11 65±9 72±9 60±8 49±14
ICA 58±5 66±8 68±10 59±9
ACA 40±11 48±9 51±10 46±11 35±11
ICA (siphon) 55±12 62±8 67±11 58±12
PCA1 36±13 40±12 42±7 39±8 33±14
BA 35±6 41±5 44±8 36±7
RI MCA 0.47±0.05 0.55±0.05 0.50±0.05 0.53±0.05 0.56±0.06
PCA1 0.55±0.05 0.58±0.05 0.55±0.05 0.55±0.05 0.54±0.06
ICA 0.52±0.05 0.60±0.05 0.55±0.05 0.58±0.05
ACA 0.55±0.05 0.57±0.05 0.57±0.05 0.58±0.05 0.56±0.07
BA 0.55±0.05 0.60±0.05 0.55±0.05 0.57±0.05
ICA (siphon) 0.57±0.05 0.63±0.05 0.55±0.05 0.58±0.05
Adapted from Bode H (1998) Pediatric applications of transcranial Doppler sonography. Springer, Wien, NewYork, 1988; Krejza J, Mariak Z, Walecki J,
PCA1 posterior cerebral artery, rst segment and BA basilar artery
Szydlik P, Lewko J, Ustymowicz A (1999) Transcranial color Doppler sonography of basal cerebral arteries in 182 healthy subjects: age and sex variability and
Normal age-dependent Resistance Index (RI) values and normal ow velocities (cm/s)±sd for systole (Vs), end diastole (Ve s ) on TCI.Time average mean
normal reference values for blood ow parameters. AJR 172:213–218
Abbreviations: Vs maximal systolic velocity, Ved end-diastolic velocity, MCA middle cerebral artery, ACA anterior cerebral artery, ICA internal carotid artery,
velocity (TAV ) and Pulsatility Index (PI) less important and not listed

124
M. Riccabona
a b
Fig. 8.9 Transtemporal DS tracing while applying fontanellar pressure. Duplex Doppler gate
placed in main MCA branch on a TCI-CDS acquisition. Note: Reduction of systolic ow velocities
and even more inverted diastolic ow direction when slight fontanellar compression is applied by
ngertip (arrow, “Font.Druck”) (a). Spectral duplex Doppler ow velocity measurements give
respective numbers (b)
• Physiologic variations in ow velocities and RI indices with change of PCO2—
used to monitor cerebral perfusion and optimise respirator settings (e.g. children
under hyperventilation for treatment of brain oedema after hypoxic events).
• Subtle mechanical fontanellar pressure used to assess effect on brain perfusion—
useful for assessment of critical intracranial pressure elevation (e.g. hydrocephalus) (Fig.8.9).
• Differences in ow velocity and RI values between intra- and extracranial portion of ICA used to demonstrate normal, slightly or signicantly elevated brain
pressure (see hydrocephalus).
8.2.4 Normal Variances inPreterm Babies
8.2.4.1 Periventricular Echogenicities
Physiologically reduced differentiation between grey and white matter due to immaturity; central nonmyelinated white matter can be relatively echogenic, particularly
in periventricular areas.
Periventricular white matter is frequently homogeneously and slightly increased
in echogenicity (often symmetric) in severely premature and very immature neonates (i.e. “PVE”=periventricular echodensity - often physiologic) (Fig.8.10).
Note Findings often difcult to differentiate from early hypoxic-oedematous
changes that eventually may lead to periventricular leukomalacia (PVL).

8 Neurosonography inNeonates, Infants andChildren
Fig. 8.10 PVE in preterm infant. Typical increased paraventricular echogenicities (“PVE”) in
severely immature brain of preterm baby. (a) Parasagittal section-the slightly patchy appearance
may indicate early PVL, only to be decided on follow-up. (b) Coronal view tilted occipitally
125
Immature brain also exhibits reduced gyration and prominent CSF spaces
(intra-/extra-axial); embryologic cavities can persist and may be remarkably
prominent, with high-resolution transducers radiate bers of the coron depictable
(Fig.8.11).
8.2.4.2 Ventricular Asymmetry
To a certain extent, this can be seen as normal variant—does not always indicate
pathology, and may also depend on/vary with head position.
8.2.4.3 Ventriculomegaly
Term neonates: ventricles measuring 5–10 mm (at level of foramen of Monro)
called ventriculomegaly.
In older children: ventriculomegaly without other signs of hydrocephalus mea-
suring up to 1.5cm axial diameter.
8.2.4.4 Cisterna Magna
Size quite variable (range 2–10mm). Large posterior fossa CSF spaces more common in preterms (Fig.8.11d, e).
Note Sometimes differentiation of large cistern (megacisterna magna) versus
arachnoid cyst or Dandy–Walker “pseudocyst” difcult or impossible.
8.2.4.5 Vascular Variations
Many anatomic variations of brain vessels without pathologic implications are
known, only some detectable by CDS.

126
M. Riccabona
a
bc
de f
Fig. 8.11 US appearance in preterm babies—typical features and ndings. (a) Parasagittal sec-
tion—wide CSF space (++). (b) Coronal section: reduced gyration + prominent periventricular
echoes with echogenic lines of the corona radiata. (c) Sagittal midline view: physiologically persisting cavum septi pellucidi et vergae. (d) Coronal midline section, posterior fossa: large cisterna
magna. (e) Sagittal midline section, posterior fossa: prominent CSF space (cisterna magna). Note
how much better posterior fossa structures and cerebellum are visualised using an occipital/nuchal
approach (f), and that image appearence also varies with equipment, presets, frequency, US technique, and transducer
Note Many systemic or cardiac conditions may inuence Doppler ndings, e.g.
heart malformations with shunt, cardiac insufciency, heart rate, drugs, hypo- and
hypervolaemia, anaemia, dehydration, hyperviscosity, altered respiration, PCO2
and increased intrathoracic pressure (Fig.8.12). Furthermore, extracranial conditions or position may affect perfusion pattern in cerebral vessels (e.g. SIDS risk in
infants with altered BA ow when head is extremely turned to the one or other
side). Thus, not all altered spectral Doppler ndings indicate brain disease or
cerebral vascular problems; however, they may hint at potential perfusion disturbances with neurologic sequelae secondary to another underlying condition.
Sometimes CDS is used to grade these conditions in terms of therapeutic needs
(i.e. grading of PDA).

8 Neurosonography inNeonates, Infants andChildren
a
127
b
d
e
c
Fig. 8.12 Impact of heart rate and extracranial conditions on Doppler ndings: different ow pattern, RI and V
whereas diastolic velocity decreases (as shown in lower spectral trace). (b, c) Flow alteration in BA
when head is turned (“Drehung”)—normal ow in normal position (“Gerade”). (d) Retrograde
ow (encoded in blue) in left vertebral artery in subclavian steal Syndrome. Duplex trace conrmation, in this example in a baby after ALTE (acute life threatening event) during extensive head
turning, with consequently inverted ow direction of basilar artery (encoded in blue) (e)
(a) Diastolic velocity changes with heart rate—RI increases with bradycardia,
diast.
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