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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
431
Role of US
• Major imaging tool for assessment and follow-up, also at bedside.
• May help decisions on additional imaging.
Additional Investigations
VCUG/ce-VUS, scintigraphy, MR urography/angiography.
Rarely CT, interventional radiology for potential percutaneous treatment.
15.6 Adrenal Glands andPararenal Space
15.6.1 General Remarks
Prominent in rst months of life (length 10–12mm), will then shrink to approximately 50%.
Thereafter constant growth over years—eventually ends in puberty with normal
size (length~2cm). Medulla prominent in neonate; cortex later becomes prominent.
15.6.2 Typical Normal US Finding
V- or Y-shape structure situated on the upper pole of the kidney (Fig.15.38):
• Shape variable, particularly in the ectopic position of the kidney.
• Centrally echoic, less echoic peripheral cortex, surrounded by more or less echogenic perirenal fat.
Note In neonates adrenal gland easy to visualise; the older and more obese a
patient, the more difcult to assess by US.
Fig. 15.38 Normal adrenal gland. (a) Normal shape and appearance of adrenal gland in neonate.
(b) Enlarged view nicely showing typical neonatal differentiation of adrenal medulla and cortex.
(c) Atypical shape of the neonatal adrenal gland due to missing right kidney

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Volume
Various methods with partially complicated calculations reported. Rough estimate
of size achieved by maximal sagittal length.
Note Differentiation of prominent adrenal gland (e.g. reactive to stress/other physi-
ologic conditions) from hyperplasia/enlargement in other conditions may be
impossible.
Normal Variations
Hypoplasia/aplasia; associated with severe hormonal decits if bilateral.
Hypertrophy/hyperplasia difcult to dene sonographically, usually in combina-
tion with clinical symptoms/syndrome and respective hormonal ndings.
Different shape and position variations (e.g. preveterbral fused horseshoe
adrenals …).
15.6.3 Pathologic Findings
15.6.3.1 Adrenal Gland Haemorrhage
Typically in newborns, asphyxia, after trauma/stress—but also with sepsis, systemic
conditions.
• May occur fetally. Varies in size, uni- or bilateral.
• May cause displacement of surrounding structures (e.g. thus impairing renal
blood ow with consequent renal vein thrombosis).
• Rupture/retroperitoneal haematoma/haematoperitoneum extremely rare.
US Findings
• Initially inhomogeneously echogenic enlargement of the adrenal gland with
shape of complex cyst (Fig.15.39).
Fig. 15.39 Adrenal gland haemorrhage. (a) Huge, fresh adrenal gland haemorrhage in a neonate
after birth trauma. (b) Same patient as in (a): CDS demonstrates normal perfusion of the adjacent
kidney (important to check, as adrenal gland haemorrhage can cause/be associated with renal vein
thrombosis); investigation a few days later, with sedimentations due to starting resorption of now
inhomogeneous appearing haematoma. (c) Calcication with shadowing of adrenal gland (++)—a
remnant of adrenal gland haemorrhage

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
433
• Then increasingly hypoechoic with complex liquid aspect, septations,
sedimentations.
• Shrinkage/resolution, potentially with some remnant calcication (echogenic,
with dorsal shadowing):
• Usually easy to differentiate from similar entities.
CDS Haemorrhagic cyst, complex dysplastic upper moiety of duplex kidney, para-
renal/subcapsular haematoma, psoas haematoma/abscess, urinoma, cystichaemorrhagic tumour.
Role of US
In neonates US the ideal method; in older children sectional imaging may become
necessary, as well as in equivocal situations (provided a therapeutic consequence).
15.6.3.2 Inflammatory Condition
May occur secondarily/haematogenously in systemic disease (e.g. sepsis,
tuberculosis).
US Findings
Unspecic enlargement with focal complex uid collections in abscess formation:
• Tuberculous abscesses may contain echogenic content, cause calcications.
Tuberculoma is rare.
Eventually difcult to differentiate from remnants of adrenal gland haemorrhage.
Role of US
May depict ndings; aetiology dened by laboratory/clinical ndings.
US-guided biopsy?
15.6.3.3 Tumours
Adrenal Cysts
Rare, potentially dysontogenetic, after haemorrhage/infection, tumourous origin.
US as in any cyst; nonspecic, may vary in size:
• Sometimes difcult to differentiate from renal cyst/cystic upper pole system.
• May cause focal mass effect, may secondarily cause haemorrhage:
• More complex aspect of cyst may raise suspicion of cystic tumour.

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Adrenal Adenoma
Extremely rare in children.
Commonly hormonally active, causing Cushing syndrome/virilisation in girls:
• The latter also associated with diffuse adrenal hyperplasia, difcult to identify by US.
No specic US ndings.
Neuroblastoma
Most common neonatal tumour, developing from medulla of the adrenal gland, may
occur prenatally, may be in all other areas with such paravertebral ganglia cells
(neck, chest, other abdomen ...):
• Low-grade tumours may spontaneously regress/disappear spontaneously, particularly if small.
• Typically associated with elevated catecholamines in urine, however, catecholamine negative variants occur as well as neuroblastoma with other hormonal
activities/respective symptoms.
US/CDS Findings
No specic US features that allow diagnosis/differentiation of prognostically varying entities. Commonly ovoid to spherical, space occupying lesion of low echogenicity, sharp margins, stippled echogenic calcications, commonly with only
little shadowing (Fig.15.40):
• Haemorrhage/necrosis possible—appearing like complicated collections/cysts.
• Commonly easily assigned to the adrenal gland.
• In large tumours differentiation from exophytic renal/hepatic tumours more challenging—use typical features (e.g. motion during breathing, compression/distortion of adjacent structures).
Fig. 15.40 Neuroblastoma. (a) Small neonatal neuroblastoma (++)—these usually only observed
and often vanish spontaneously; urine catecholamine metabolites tested for proving diagnosis. (b)
Neuroblastoma (
2
ment (
++); note still-preserved parts of the adrenal gland on the left upper aspect adjacent to
tumour. (c) Large neuroblastoma in 3-year-old child exhibiting typical calcications and causing
mass effect; thick slab rendering of a 3DUS acquisition enhances those calcication, though inducing some blurriness
1,3
++) in an infant arising from paravertebral ganglia, with regional node involve-

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
435
• CDS may show intratumoural vessels.
• Origin of vessels helpful for differentiating origin of tumour.
• Central vessels help differentiation against haemorrhage, although haemorrhagic
tumours will also not exhibit vasculature in haemorrhagic/necrotic parts.
Staging
Different staging used in different parts of the world, generally performed by sectional
imaging; additionally based on histology/surgery ndings. Main features: size, location, resectability/invasion of adjacent organs/structures, focal lymph node involvement, systemic metastases (particularly liver assessable by US). Risk stratication
also heavily relies on histology and genetics (i.e. mutations, nyc1 amplication ...).
Note Neuroblastomas occur also in other body areas (from neck to pelvis) within
remnants of neurogenic crest—mostly in paravertebral ganglia. In these less typical
locations more difcult to depict (in suspected neuroblastoma actively search all
these locations). Tend to invade neuroforamina/spinal canal, displace/encase retroperitoneal vessels.
Ganglioneuroma
Usually occurs in paravertebral ganglia, more benign variant of neuroblastoma, not
distinguishable by US (Fig.15.40).
Phaeochromocytoma
Rare tumour in infancy/childhood, arising from adrenal medulla/sympathetic paravertebral or paraaortal ganglia (neck to pelvis). Typically associated with elevated
blood pressure/respective hormonal ndings.
May be familial/combined with other entities (e.g. sarcomatosis, multiple endo-
crine neoplasia, and bilateral manifestation).
US Findings
Well-dened tumour with sharp borders, sometimes somewhat inhomogeneous,
intermediate echogenicity. Parenchymal calcications/areas of increased echogenicity are possible (Fig.15.41).
Entity not dened by US but by associated clinical symptoms/hormonal (lab-
Note
oratory) ndings.
Adrenal Carcinoma
Extremely rare in childhood, very aggressive, arises from cortex, may be hormonally active.
US Findings
Usually hypoechoic, more or less homogenous, aggressive mass inltrating surrounding structures, even penetrating diaphragm/into pleural space. Early metastases locally and systemically, may invade vessels. No specic other signs.

436
Fig. 15.41 Other adrenal
tumours. (a) Enlarged
adrenal gland with atypical
appearance in
adrenogenital syndrome/
congenital adrenal
hyperplasia. (b) Adrenal
gland tumour in child with
severe hypertension:
pheochromocytoma
M. Riccabona
Role ofUS
Screening method in all conditions with potential adrenal gland involvement, such
as hormonal symptoms, virilisation, precocious puberty, adrenogenital syndrome,
signs of acute haemorrhage (e.g. after asphyxia, unexplained neonatal anaemia) and
hypertension.
Furthermore used for follow-up.
For DDx/tumour staging, sectional imaging mandatory; in neuroblastoma
include MIBG scintigraphy. Always search for tumour-specic metabolites in urine
and blood (catecholamines).
15.7 US ofUrinary Bladder
15.7.1 Requisites
Sufcient bladder lling is essential:
• If not achievable by drinking, consider catheterisation with instillation of saline.
• For assessing potential VUR, additional instillation of UCA feasible (ce-VUS;
see there).
Note Always assess before and after voiding; consider US during voiding using
perineal transducer position for urethral assessment. Always include paravesical
space/collecting system of both kidneys before/after voiding.
Transducers
Commonly curved linear arrays used—also for detailed assessment of urethra during voiding (perineal US), measurement of bladder wall; linear transducers are
also used:
• Difcult access: small footprint sector transducer may be an option.

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
437
• Neonates/infants: (additionally) high-resolution linear transducer, particularly
also for urachus assessment.
How to Assess
Always assess bladder in longitudinal and transverse sections (see Fig.15.2):
• Oblique sections through area of ostium (used to visualise distal/transmural
ureters).
Actively evaluate trigone, bladder neck, ostium, bladder wall, and bladder roof
(urachal remnants):
• Include paravesical space (internal genitalia, ascites, etc.).
If possible/indicated: add perineal sagittal sections for urethra (vagina)
visualisation:
• Bladder wall measurements should always be taken in sufciently full bladder,
never at trigone; should generally not exceed 2mm in full bladder (otherwise
cut-off=4mm).
• Bladder size/volume calculation: standard ellipsoid eq. (L×W×H) using vary-
ing correction factors—depending on bladder shape (0.5 for spherical/ellipsoid
conguration, 1.0 for rectangular shape). See above.
Fig. 15.42 Bladder pathology. (a) Trabeculation of the bladder wall in a neurogenic bladder. (b,
c) Small (b) and large (c,
increased intravesical pressure (same patient as c) causing aberrant voiding
1
+…+) diverticulum. (d) CDS shows urine inux into diverticulum with

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M. Riccabona
• Normal bladder volume varies with age; simplied estimation of age-related
bladder volume=[age (in years) +2]×30 (mL).
Always pre−/post-void volume should be compared, difference calculated to
assess pathologic residual volume (>10%/>20mL).
• Physiologically residual urine noted in neonates (immature bladder function)
and after nonphysiological voiding situations.
Ureteric inow may be seen on gray scale, particularly if urine very concentrated
of with cellular content:
• CDS will improve depiction of ureteric jet, which usually should be symmetric
and regular—helps depiction of asymmetric ostium position or asymmetric urine
inow (see Fig.15.2).
Note All respective sections have to be documented.
15.7.2 Pathologic Findings
15.7.2.1 Atypical Shape (Neurogenic Bladder, “Valve Bladder”)
Nonphysiologic tension even with little lling, volume, signs of dysfunction (open
bladder neck), thickened trigone, thickened bladder wall, reduced/enlarged capacity, trabeculation, pseudo-diverticula; atypical position/number/shape of ostium
(e.g. gapping ostium), etc. (Fig.15.42):
• (Secondary?) Dilatation of distal ureter with stenosis by thickened bladder wall,
ureteral junction stenosis (obstructive megaureter—UVJ obstruction, see below),
dysplastic/immotile segments, obstructing concretions
15.7.2.2 Polyps
Arising from the wall or entering through bladder neck (urethral broepithelial
polyps).
May exhibit central vessel arising from the bladder wall (Fig.15.43).
15.7.2.3 Bladder Tumours
Rare in children.
Either diffusely inltrating wall with wall thickening (e.g. neurobroma), arising
from wall/growing into lumen or into paravesical space in cauliower-like appearance (mostly rhabdomyosarcoma) or also arise from adjacent structures inltrating
bladder (e.g. from prostate/vagina).
US nonspecic may exhibit vascularity (Fig.15.44).
DDx: clots/brin (may be adherent to wall, then positioning manoeuvres do not
help for differentiation, as they then do not change position), pseudotumours in
atypical or haemorrhagic infection, polyps.

15 Ultrasound oftheUrogenital Tract inNeonates, Infants, andChildren
Fig. 15.43 Bladder polyps. (a, b) Typical polyps of bladder wall (++) with typical vascular ped-
icle depictable by aCDS (a) or CDS (b). Bl bladder. (c) Polypoid structure (++) reaching into the
bladder through bladder neck, in a child with a broid polyp of the posterior urethra
439
Fig. 15.44 Bladder wall (pseudo)tumours and DDx. (a) Bladder rhabdomyosarcoma: cauliower-
like polypoid tumour growing into bladder lumen, with broad attachment to the bladder wall. (b)
Regional thickening of the bladder wall in a child with neurobromatosis Type I, consistent with
bladder wall neurobroma (++)
Fig. 15.45 Bladder wall calcication.
Echogenic inner layer of thickened
bladder wall in amoebiasis
15.7.2.4 Calcification in/of Bladder
Typically in advanced schistosomiasis—with an echogenic layer in thickened bladder wall, usually with reduced bladder capacity/increased bladder tension
(Fig. 15.45). Also urolithiasis may occur in bladder after passing from above or
(infectious) stones grow in bladder (e.g. after / during infection, in cystinuria…).
DDx: thickening of bladder endothelium in inammation (cystitis) with freeoating particles in lumen, bladder sedimentation (blood, proteins, cells,

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concentrated urine, crystals, concretions—particularly large stones in oxaluria/cystinuria, etc.).
15.7.2.5 Ureterocele
Cystiform end of ureter protruding into the bladder lumen at ostium:
• Orthotopic ureterocele usually draining single renal system, central opening.
• If associated with duplex kidney, then typically positioned at more distal-medial
position entering ureter that drains the upper moiety of duplex system, often
causing megaureter. Usually have opening at mediocaudal aspect of
ureterocele.
US/CDS Findings
• Cystic structure protruding into the bladder of varying size.
• Large ureteroceles may herniate into the bladder neck causing obstruction during
voiding (Fig.15.46).
May also drain ectopically, protrude into vagina or paravesically/proximal ureter,
seminal vesicles, etc.
a
def
Fig. 15.46 Ureterocele. (a) Typical image of a ureterocele protruding into the bladder lumen like
a cyst at site of the ostium. (b) Parasagittal oblique section through ureterocele depicts corresponding megaureter (++) behind bladder. (c) Small collapsed ureterocele in an insufciently hydrated
child—only some ostial irregularity and thick wall of ureterocele (++) depictable by meticulous
scanning. (d) Ectopic ureterocele (
thra. (e, f) ce-VUS in a duplex kidney with ureterocele: observe non-contrasted ureterocele (UC)
with respective megaureter (MU) (e), contrast reux into the other dilated ureter (U) up to grossly
dilated lower moiety (f, oblique section)
+…+) behind bladder, potentially draining into vagina or ure-
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