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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

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
401
a
d
f
bc
e
g
*
*
Fig. 15.20 Pop-off urinoma with renal dysplasia. (a) Dysplastic kidney in neonate with PUV,
dilated pelvis, and dysplastic cysts. (b) Complex uid formation adjacent to relatively normal
looking kidney in PUV, consistent with calyceal rupture and pop-off urinoma which seems to have
a protective effect reducing renal damage. (c) Same neonate as in (b): good vascularisation of renal
parenchyma, large urinoma in front of kidney. (d) Dual/split image technique, dorsal axial scan
through both kidneys including aCDS: obviously signicant difference in renal size and perfusion,
left kidney severely damaged (same can also be seen in other patients with high-grade VUR without PUV) (e) Urinoma of right duplex kidney in a baby with ureterocele (*) (f), also obstructing
bladder outlet which is best seen in a perineal view (g) and not just the respective upper moiety—
after rupture of the upper moiety’s calix (arrow)
• Renal function assessed by DMSA scintigraphy (best results after approx. Third
month of life—as it only works with sufcient renal function after renal imma-
turity has ceased).
• Rarely MRU (in additional complex pathology).
• No indication for IVU.
Vesico-Ureteric Reflux (VUR)
Definition
Insufcient urinary ostia (primary/secondary); reux of urine from bladder to ureter/renal collecting system—with more or less dilatation of ureter and/or calyceal
system. Grading I°–V° according to international classication.

402
M. Riccabona
US Findings
Indirect signs in bladder: bladder wall thickening, trabeculation, lateralisation of
ostium, and gaping ostium. Varying dilatation of ureter that may exhibit wall thickening. Post-void increase of dilatation of collecting system and pelvic urothelial
thickening (Fig.15.21).
CDS
Ureteric inow jet may be atypical, asymmetric, and originate from lateralised ostium.
Fig. 15.21 Vesico-ureteric reux. (a) Left kidney, axial view before voiding: no distension of
collecting system/renal pelvis. (b) Same girl, same section after voiding: signicant widening of
the renal pelvis indicating dilating VUR. (c) Urothelial sign: thickened wall of non-distended renal
pelvis—a nonspecic sign for VUR, involvement in UTI, obstruction, congestions, etc. (d) Duplex
ureter—the upper and more lateralised ostium (draining lower moiety of respective kidney) is gapping, indicative of VUR. (e) ce-VUS shows contrast reux into proximal ureter and renal collecting system. (f) Comparison of two kidneys in same patient showing different size and pelvic wall
thickening associated with different degree of VUR

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
403
Sometimes, particularly with particles in urine, VUR can be directly visualised
by reversed colour ow signals in ureter.
Note These have to originate from within bladder through ostium—as otherwise
reected retrograde ow from closed ostium may mimic VUR.
ce-VUS (see also respective entry and chapter): reux of US contrast agent into
ureter/pelvicalyceal system—with more or less distension, depending on VUR
grade. Grading of VUR achievable by ce-VUS (correlates with standard VUR grading on VCUG).
Note Always assess renal parenchyma for signs of dysplasia/scars after
infections.
Connatal dysplasia in severe VUR (common in baby boys, PUV) called “congenital reux nephropathy.”
Postnatally VUR itself does not cause renal damage, only in conjunction with
recurrent upper UTI.
Additional Investigations
VCUG—particularly in boys, preoperatively, for detailed analysis not only of urethra (also ureter, potential diverticula…). Rarely bladder function studies are
performed.
DMSA scintigraphy for assessing renal parenchyma damage (might be replaced
by MR in future).
IVU outdated.
Secondary Obstruction
Definition
Number of causes such as urolithiasis or compression (by tumours, retroperitoneal
brosis, etc.).
US Findings
Acute obstruction usually does usually not exhibit signicant dilatation—unless
there is preexisting chronic drainage impairment/other forms of dilatation.
Increased echogenicity of parenchyma and swollen and enlarged kidney.
Potentially perirenal oedema/stranding.
Concretions/stones (urolithiasis): usually echogenic structure with dorsal
shadowing, distended collecting system or ureter narrows after level of
obstruction.
CDS
In acute severe obstruction, there is diminished peripheral vasculature (a)
CDS.Asymmetrically elevated RI in acutely obstructed kidney.

404
ab
M. Riccabona
In total obstruction, lack of ureteric inow jet from affected ureter—otherwise
asymmetric (even ipsilateral dominant) ureteric jet (e.g. from haematuria).
Twinkling sign from stone (Fig.15.22).
Role of US
Perfect initial diagnostic tool:
• In children, stones can be visualised in nearly all parts of urinary tract, par-
ticularly in kidney, at pelvi-ureteric junction, in distal ureter—provided suf-
ciently lled bladder allows access. Even urethra (by perineal US)
(Fig.15.22d).
Note Following dilated ureter downwards from renal pelvis will often allow
depiction of obstructing stone even in mid/lower ureter, e.g. at pelvic vessel
crossing.
Furthermore initial US allows tailoring of further examinations. Adjacent compressing structures can usually be visualised, too; potential for US-guided
intervention.
c
Fig. 15.22 Twinkling sign/ureteric stone. (a) Distal ureteric stone (1+…+) with some dilatation
of ureter and only little shadowing, only depictable with sufciently lled urinary bladder. (b)
Urethral stone (
patient as b). (d) Pelvic oor rhabdomyosarcoma, visualised through bladder (
presses+displaces urethra (U,
1
+…+) depicted by perineal US. (c) Twinkling sign caused by urethral stone (same
1
+…+), causing urethral obstruction
d
2
+ …+) com-

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
405
Additional Investigations
• Kidney-ureter-bladder lm (KUB).
• Focused IVU or stone CT (particularly in complex and equivocal situation where
it is increasingly preferred):
– Not indicated with same frequency as in adults—due to radiation burden.
• Role of MR is yet undened.
• See also ESPR/ESUR recommendations—Pediatr Radiol (2010) 40:1315.
15.3.2 Inflammatory Renal Parenchymal Conditions
Role of US
Perfect initial diagnostic imaging method and for follow-up (and US-guided biopsy
for DDx).
Additional Imaging
DMSA scintigraphy in acute or chronic setting (for scars, wait 4–6months after
infection):
• Complicated infections or DDx of pseudotumours may require MR (or CT, if
MR is not available).
• IVU usually not indicated in children (rare exceptions, e.g. unless there is a sus-
pected obstructing stone).
• Additional nephro-urologic work-up of potentially underlying/associated condi-
tion recommended.
• Imaging algorithm for paediatric UTI: see ESPR/ESUR recommendation Pediatr
Radiol (2008) 38:138.
15.3.2.1 Pyelitis
Definition
In children isolated pyelitis is rare—potentially associated with VUR.Commonly
associated with interstitial bacterial nephritis.
US Findings
Thickened echogenic renal pelvic wall and echoes within collecting system, which
tends to be enlarged, hypotonic, and wide (Fig.15.23).
Secondary stone formation or fungus may be present; fungus usually similar to a
stone, often larger and somewhat polygonal shaped; dorsal shadowing less than
with a typical concretion, may cause secondary obstruction.
15.3.2.2 Acute Pyelonephritis (aPN)/Interstitial Nephritis
Definition
Haematogenous or ascending infection, bacterial or viral, sometimes atypical
(tuberculosis).

406
bc
M. Riccabona
a
de
Fig. 15.23 US in urinary tract infection (UTI). (a) Echogenic content oating throughout bladder
in UTI. (b) Echogenic debris (clot and brin) sitting at bladder base in haemorrhagic cystitis. (c)
Enlarged kidney, with swollen urothelium of lax and slightly distended renal pelvis in an infant
with upper UTI (acute pyelonephritis). (d) Enlarged kidney with disrupted cortico-medullary differentiation and increased echogenicity in upper UTI with diffuse renal involvement. (e) aCDS
depicts multi-segmental perfusion defects in same child as (d); these local manifestations were less
depictable on gray scale US
US/CDS Findings
Focal/diffusely altered parenchymal echogenicity—commonly increased, swollen
kidney, in focal infection even pseudotumours, regional swelling (“lobar nephronia”), peripelvic increased/broadened echogenicity and perirenal oedema, often
associated with ndings as in pyelitis.
Regionally/segmentally decreased vascularity—particularly well seen on aCDS,
diffuse asymmetrically reduced vascularity on power Doppler in diffuse infection
(Fig.15.23).
15.3.2.3 Necrosis andAbscess Formation
US/CDS Findings
Increasingly inhomogeneous defect, hypoechoic structural alteration with eventually complex cystic conguration and rim-like margin; may resemble complicated cyst.
Focal perfusion defect, potentially capsular hyperaemia (Fig.15.24); CEUS may
enhance depiction and aid DDx.

bc
15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
407
a
d
Fig. 15.24 Complications in UTI, DDx, scarring. (a) Focal necrotic cortical area (+…+) seen as
hypoechoic spheric lesion in severely prolonged upper UTI; note also broadened peripyelonal
echogenicity and hazy cortico-medullary differentiation of swollen kidney. (b) Multiple necrotic
(dark) segmental defects throughout kidney in severe diffuse/multifocal necrotising pyelonephritis. (c) Same patient as in (b): aCDS demonstrates only minimal residual central perfusion—eventually entire kidney had to be removed. (d) Spheric focal complex liquid lesion in a child after UTI,
with sparing of vessels on aCDS–consistent with early appearance in formation of an renal abscess
15.3.2.4 Scarring
US/aCDS Findings
• Regional narrowing of parenchyma with contour alteration, disrupted/abnormal
cortico-medullary differentiation, and clubbing of affected calix.
• Regional small strip-like defect, particularly well seen on aCDS (Fig.15.25).
15.3.2.5 Tuberculosis
US/CDS Findings
Necrosis/atypical abscess—echogenic content, potentially with partial rim-like calcications, commonly similar as complicated cyst. No other specic US/aCDS
ndings.
15.3.2.6 Xanthogranulomatous Pyelonephritis
Definition
Chronic infection, often with obstructive concretion/stone (“staghorn” shaped) that
leads to destruction of medulla, eventually of entire kidney.
US/CDS Findings
Regionally or diffusely thinned parenchyma and vasculature (aCDS), peripheral
hyperaemia in membrane around abscess formation. Pseudotumourous aspect of

408
Fig. 15.25 Scarring. (a) Focal scar with clubbed calyx and destroyed cortex after the upper pole
aPN. (b) Small peripheral scar (++) seen as perfusion defect on aCDS, not easily depictable by
gray scale US
M. Riccabona
Fig. 15.26 Xanthogranulomatous pyelonephritis. Xanthogranulomatous pyelonephritis in a child
with distal renal acidosis and stone disease, longitudinal (a) and axial (b) section: complex cystic
destruction of medullae, central calcications, tumourously enlarged kidney, shape somewhat
preserved
destroyed affected part. Disruption of normal renal parenchymal and vascular architecture in abscess and necrosis; potentially perifocal hyperaemia around kidney
(Fig.15.26).
15.3.2.7 Glomerulonephritis/Nephrotic Syndrome
Definition
Large range of conditions.
US Findings
Commonly increased renal size, small medulla, enlarged cortex, and potentially
increased echogenicity/reduced cortico-medullary differentiation, depending on
which compartments involved (Fig.15.27).

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
Fig. 15.27 Glomerulonephritis. (a) Swollen large right kidney (+ +) with small hypoechoic
medullae in acute but mild (postinfectious) GN (ndings bilateral, renal function normal). (b) A
less-enlarged but still slightly swollen kidney with hyperechoic parenchyma and reduced corticomedullary differentiation in chronic recurrent GN (HUS may appear similar)
409
Typically bilateral ndings:
• In chronic stage, kidneys may be small.
• In mild/atypical disease, kidney may look normal.
• Differentiation between various entities sonographically impossible.
• Other systemic ndings: ascites, pleural effusion—depend on degree of renal
failure/associated condition.
Consider renal manifestation of systemic disease such as lupus, Henoch–
Schonlein purpura, amyloidosis, familiar Mediterranean fever, etc.
CDS Findings
Diffuse perfusion alterations—correlate more with degree of renal failure than with
underlying entity (except for primarily vascular conditions—see below).
Role of US
Initial diagnosis: exclude other conditions by validating pre-/postrenal causes of
renal failure. Assessment of renal perfusion, also during course of disease, as well
as secondary/associated changes (e.g. under haemoltration—intravascular
volume?).
US-guided biopsy for histological evaluation (see respective chapter too).
15.3.3 Vascular Conditions
Role of US in Renal Vascular Conditions
Most developed tool for screening, initial diagnosis, and follow-up. US most useful
for follow-up, differentiation against other renal conditions, and monitoring of
future renal growth.

410
M. Riccabona
Will allow depiction of changes in perfusion patterns:
• However, if US potentially limited, then additional imaging necessary (see above).
• Algorithms recommended for certain conditions, e.g. imaging in suspected
childhood renovascular hypertension (see Pediatr Radiol (2010) 40:1315).
15.3.3.1 Renal Artery Stenosis
Definition
Rare in childhood, commonly not arteriosclerotic in origin but associated with other
vasculopathies, after vasculitis, trauma/surgery, by compression.
US Findings
• Using meticulous scanning techniques, entire course of extrarenal artery is often
visualised.
• Rarely changes in diameter or aneurysmal dilatation seen on gray scale.
• Intrarenal portions only assessable using CDS.
CDS
• Most striking nding: aliasing of colour spectrum—provided adequate scale
settings.
• Always perform spectral analysis:
– At level of stenosis: marked increase in systolic velocity with spectral broad-
ening+turbulent ow.
– Distal to stenosis: decreased systolic velocity, more or less normal to elevated
diastolic velocity, depending on severity/grade. Delayed systolic upstroke
with increased acceleration index (pulsus tardus et parvus) (Fig.15.28).
– In kidney: sometimes aCDS depicts segmental hypoperfusion due to infarc-
tion of affected area after severe stenosis.
Fig. 15.28 Renal artery stenosis. Elevated ow
velocity with turbulent atypical ow at site of the
left renal artery stenosis, also seen as aliasing of
CDS signals and narrow vessel diameter. Note that
at stenosis no attening of systolic upstroke may
be present in the spectral Doppler trace
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